When asked what substance he was first addicted to, guitarist Eric Clapton answered: “sugar.”  And we all know the person who kicked the “hard drugs” only to become reliant on food as their “go-to” addiction of choice.

So, are we all doomed for food addiction?

Well, 97% of people prescribed opioid painkillers (with no history of addiction) don’t become addicts.  And most of us wouldn’t rob a 7-11 for candy bars if the price of candy bars became unaffordable.  But some people are more susceptible to addiction, whether it’s opioids or candy bars.

Thus, addiction is complicated: Social, motivational, emotional, and genetic factors all interact to create an addiction experience. An addictive substance alone doesn’t create addiction. However, some things are more addictive than others.

We often joke “I’m a ___ addict”, whether that’s video games, shoes, or ice cream. But what, exactly, is real addiction? And is it a useful concept for understanding food behaviour?

What is addiction?

Addiction is an overpowering craving to repeatedly engage in an activity that provides temporary relief at the expense of terrible consequences. It’s something you feel compelled to do, even though it harms you.

To count as an addiction, there must also be withdrawal — feelings of discomfort, distress, and intense cravings – when our addictive substance or behaviour is taken away or stopped.

What is food addiction?

Thus, food addiction involves a regular compulsion to eat and/or consume particular foods, even though those foods harm us — whether that’s because the foods are unhealthy (e.g. high in sugar), or because they make us sick, or cause us to become obese.

An occasional big meal: not addiction. Regularly eating so much, and so rapidly, that you end up bloated and nauseated — but feel unable to stop? Potential addiction.

After having a couple of cookies (or any potentially addictive food), a non-addict will feel indifferent about eating more.  The experience of an addict is much different.  Addicts become utterly single-minded in the pursuit of their “hit”. Eating a couple of cookies (or any potentially addictive food) sets off an abnormal reaction – and they want more and more until they’re physically unable to swallow.

If you aren’t an addict, it’s not that you are a master of self-control, you just don’t have an insatiable appetite for more.

A food addict can be:

• an overweight woman who is always trying a new diet
• a man who eats beyond fullness at dinner after snacking on junk food all day to help deal with job stress
• a thin woman who never eats enough and is hungry all the time because she’s afraid of getting fat (in this case, her “hit” is not eating)
• a lonely guy with nothing to do on a Friday night except watch TV and eat several bags of chips
• a person who snacks all day to ease the boredom of an un-stimulating life
• a perfectionist who is never quite satisfied with their body
• a person suffering from a nutrition related disease (e.g., heart disease, diabetes, etc.) who gets disturbingly resistant when presented with treatment approaches

Some food addicts eat too much; some don’t consume enough.  For a food addict, food provides the fun, entertainment, control, reassurance, or love that’s missing in their life.  Food may also help to numb difficult emotions like fear and sadness.  Some people even have addiction to restriction.

The Yale Food Addiction test is a clinical tool for assessing food addiction (click to download in PDF).

Food dependence

But here’s the problem with determining food addiction: Unlike, say, heroin or gambling, we need food to live. Without an innate desire for food, we can wave bye-bye to evolution.

At what point does “big appetite” end and “food addiction” begin? And can you technically become “addicted” to something you need?

Researchers, while divided on the exact definition of “food addiction” or whether it truly exists, nevertheless agree that addiction is a pattern of behaviour characterized by things like:

• near-constant searches for a “hit”
• an intense compulsion and/or desire for the substance or behaviour
• strong, all-encompassing focus on getting that “hit”
• withdrawal symptoms when the “hit” is taken away
• needing more, or more intense “hits” as tolerance develops over time

By this definition, nearly anything — including food, water, or sex (i.e. things that are part of basic biology) — can be an addiction.

So let’s call it “food dependence”.

Over time, food (substance) dependence often becomes less about the high and more about preventing the negative feelings that come from abstinence.  The ability to get pleasure from the food becomes more difficult, because small amounts of the same food aren’t as rewarding.

Substance dependence: Official definitions

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) defines “substance dependence” as 3 or more of the following 7 symptoms occurring within 1 year. We’ll look at how these might relate to food dependence.

Symptom 1: I use more over time.

Over time, tolerance increases.

Food example: When I used to buy groceries, I would take them home, eat a snack and go on with my day.  Now I buy groceries and I eat all day long until I have gone through half of what I bought.

Symptom 2: I have withdrawal symptoms.

I now take the substance to avoid withdrawal.

Food example: I eat processed snacks to correct being tired and/or depressed.  To fix anxiety, I eat something crunchy, like chips or crackers to calm myself. I am afraid if I stop using food to correct my emotions, I will have nothing else to turn to.

Symptom 3: I use more than I intend.

Food example: One bowl of ice cream turns into 2 bowls, then 3 bowls.  I start with one handful of chips and end up eating the whole bag.

Symptom 4: I’m trying or have tried to cut back.

I want to reduce my intake, and I’ve tried, but haven’t been successful.

Food example: I have tried to cut down or stop my eating, but it’s always on my mind and I find a way to defeat myself, even making a special trip to get a candy bar or chips.

Symptom 5: I spend time pursuing, using, or recovering from use.

I spend a lot of time on activities necessary to obtain the substance, or recover from its effects.

Food example: I will have a list of chores to do on Saturday.  I will go to the store and buy groceries and spend the rest of the day eating what I bought, taking antacids, and sleeping.

Symptom 6: I miss important activities because of my substance use.

I miss or give up important social, occupational, or recreational activities.

Food example: I come home and eat.  Then, I’m too full to exercise or meet with friends.

Symptom 7: I eat despite knowing the consequences.

I continue to abuse the substance despite knowing it’s giving me a persistent or recurrent physical or physiological problem.

Food example: I eat in spite of horrible knee pain from obesity.  I’m so uncomfortable after a binge that I can’t lay down without regurgitation into my esophagus.  My blood pressure is high.  I’m miserable.  I am embarrassed and afraid about being in social situations but I overeat anyway.

Time magazine graphic: Addiction: What happens in the brain?

What influences food addiction?

Many factors play a role in the development of food addiction.

Fear: Addicts may fear eating a reasonable amount of food, getting fat, and/or experiencing uncomfortable emotions and hunger.

Chronic overeating: Eating too much of highly processed foods can stimulate brain opiates — “feel good” chemicals. Regular bingeing might create a dependency on this “natural high”.  We become dependent on a highly processed diet to feel “normal” and experience withdrawal symptoms when we don’t eat it.

Food restriction: What if I told you that starting tomorrow you could never have ice cream again?  What would you do today?  Probably eat a bunch of ice cream – right?  Cravings and reward responses from food are greater after a period of food restriction (whether real or imagined) and/or nutrient depletion. This is why diets and extreme restriction almost inevitably lead to binges.

Stress: Various forms of stress can trigger addiction. Binging + food restriction + stress = a winning combination for food addiction. Addiction can lie dormant when things are going well, then rear its ugly head when life trouble strikes.

Depression: Depression usually changes appetite, hunger, and fullness signals, as well as sleep patterns (normally, good quality sleep helps us manage urges — sleep is “willpower fuel”).

Weak satiety mechanisms: Some people who struggle with food addiction aren’t as tuned in to their fullness cues. They “hear” hunger signals more loudly than satiety signals.

Automaticity: Food behaviours can be strongly ingrained habits that “wear a groove” into our nervous system. Some argue that they can’t be eliminated — just rendered dormant (temporarily).

What makes food addictive?

Are all pleasurable foods automatically addictive?  Probably not.

Hyperpalatability

Processed foods are engineered in ways that exceed basic reward properties of traditional whole foods, making them hyperpalatable.

Consider items such as ice cream, burgers, candy, melted cheeses, buttery/oily sauces, and so on – these are the foods that stimulate the release of opioids and dopamine in the brain and have addictive potential (note: artificial sweeteners can even trigger a dopamine response).

Rodent studies confirm this: Rats are unlikely to binge on normal rat chow. But when given the option of sweeter and fattier rat chow, rats go on a bender.

The table below shows the characteristics of some “normal” foods and some hyperpalatable foods. Notice how much higher in sugar, fat, and/or sodium the hyperpalatable foods are — and how many ingredients each food contains.

What differentiates regular from hyperpalatable foods? Source: Gearhardt AN, et al. Can food be addictive? Public health and policy implications. Addiction. 2011;106:1208-1212.

Other things can contribute to the addictive potential of food:

Quantity: When served more, we eat more.

Processing & energy density: The right mix of fat, sweeteners, flours, caffeine and salt provides a strong reward.  Plain sugar packets or a bottle of olive oil aren’t very desirable.  Processed foods have combinations of ingredients not found in nature.  Many food components, like drugs, are not addictive until extracted and concentrated by modern processing (a whole grain vs. white flour in cake, a whole fruit vs. sugar in cookies, cocaine vs. cocoa leaves, opium vs. poppies, etc.).

Variety: When there are different colours, sizes, shapes, tastes, and textures, we eat more.  People will eat more cookie dough ice cream versus plain vanilla and more trail mix versus plain raw almonds.

Nutrient composition of foods: When we eat nutrient-poor foods, we may end up eating more overall food in order to meet nutrient needs.

Access: The number one factor in addiction is availability.  If the substance isn’t available, we can’t develop an addiction.  When the substance is readily available, addiction will be more common (think: cigarettes in vending machines).

Cultural norms: When a behavior/substance is accepted within a group, it’s unlikely that behaviour will stop. Many folks cut down on or quit smoking when jurisdictions outlawed smoking in restaurants and bars.

Individual preferences

Think about what foods have an “addictive” potential for you.  It’s important to consider these questions because any one food isn’t universally “addictive.”

• What foods do you crave?
• What foods do you think about you aren’t physically hungry?
• What foods do you want to eat more of, even when you’re full?
• What foods do you typically deprive yourself of — but later, feel unable to control yourself around?
• What foods have emotional associations for you — say, foods you remember from childhood, or foods that seem to have “special powers” to make you feel better?

Answers to the aforementioned questions don’t usually include barley, pears, asparagus and black beans (but it’s possible).

While whole foods in their most unprocessed form are still potentially addictive (think sweet fruits and fatty nuts), the potential for true dependence/addiction is low compared to processed foods (such as fruit candies and flavoured fatty nuts).

Treating addiction

People aren’t responsible for having an addiction, but they are responsible for dealing with it.

To treat addiction, you must address the following factors:

Food availability and environment

If you feel out of control with certain foods or in certain situations, you probably are.

Our behaviour depends heavily on social and environmental cues. We can adjust our behaviour by adjusting cues from our routine and environment.

Thus: Avoid people, places, and things that trigger addiction. Use social pressure to your advantage. Addicts don’t like to use their drug with sober people staring at them.

The more available — and socially acceptable — an addictive substance is, the easier it is to get hooked. Make it hard to get.

Emotions

Food doesn’t help resolve emotions. And emotions aren’t a bad thing. They actually serve a useful purpose in life and can indicate that something is out of balance.

Food can be used as a coping mechanism for emotions that feel intolerable. Once a “food rush” wears off, we’re left with the very same emotional problems… plus the additional problems addiction brings.

Many addictions stem from uncontrolled stress combined with food restriction. If these two factors can be controlled, food addiction might also be controlled.

Pharmaceuticals

What about appetite suppressants and drugs that eliminate the high from addictive foods?  These so-called solutions open up new problems (e.g., undereating, malnutrition, etc).

Compliance to pharmaceuticals like naltrexone (blocks the high someone gets from a drug) and antabuse (makes someone sick if they drink alcohol) tend to be poor.  Why?  Because people want the high again.  Even if an appetite suppressant drug is developed, the food addiction will still remain.  This has little to do with the addictive food itself and more to do with a deficiency elsewhere in life – boredom, loneliness, anger, lack of stimulation, lack of purpose, etc.

Cravings die as a side effect of changing our life and identity — medication is, at best, only a partial and temporary solution.

However, pharmaceuticals that may be useful in addiction recovery include those that treat underlying conditions leading to emotional distress (pain, depression, etc.).

Abstinence

While we can’t choose to be addicted, we can choose to abstain in order to sustain recovery. Some claim that as an addict, it’s easier to give up the addictive substance entirely than to negotiate with it.

In this case, freedom comes when we give up effort to control the substance and become abstinent. Recovery from addiction means having the restoration of choice.

However, abstinence means that addicts must be willing to face discomfort. Luckily, the longer an addict remains abstinent, the more biological urges for the substance fade. Withdrawal is worst in the beginning.

If urges return, they’re often the result of conditioned reflexes and/or the desire to escape emotional distress. Managing stress and knowing “triggers” is thus an important part of recovery.

Meaning

Recovery from addiction needs meaning and purpose.  Without meaning, there is no reason to remain abstinent.

External meanings (e.g., how the body looks, a spouse, a friend) can be fleeting.  We love them one day, hate them the next.

If we count on external meanings for sustained change, there’s a good chance we’ll be dissatisfied. Dissatisfaction fuels resentment, and soon enough we remember that overeating is a quick way to forget about the entire mess.

Meaning is one of the reasons why the idea of a “higher power” in many addiction recovery programs is appealing.  A higher power isn’t fleeting, it’s eternal. However, what’s most important is that the meaning and purpose is internal — it comes from the inside and reflects the person’s deeper values and life priorities.

Getting a handle on food addiction often requires a temporary hiatus from mirror and scale obsession. Instead, we must prioritize what’s going on inside.

Dieting

Reason is no match for addiction. Addiction is mostly an emotional-biological phenomenon.

Thus, addicts tend to be unable to rely on self-control alone — which doesn’t mean they are “weak”. (In fact, given how hard most food addicts try to change — even if unsuccessfully — arguably their will is very strong.)

The struggle with food addiction often leads to dieting, over-exercising, purging, drugs, binging, and weight gain/loss.  These are efforts to control the addiction, but these efforts are often unrealistic, become lenient, and eventually fail (and this failure can lead to more addictive behaviors). In fact, restriction and obsession with “fixing the problem” itself can create more rebounds.

Structural changes

“Willpower” helps, but it’s weak compared to structural and foundational changes. This includes things like:

• changing one’s physical environment
• building a social support system (including getting away from people who enable the addiction)
• making it tougher to get at the addictive substances
• decreasing life stress, and/or working on stress management
• learning to tolerate discomfort, and getting support in doing so
• changing one’s routine and schedule to favour positive behaviours, and diminish the chances for negative behaviours (which can include things like getting more sleep, seeking out safer situations during “trigger times”, scheduling activities that conflict with the addictive behaviour, etc.)

Other tidbits and factoids

Food addiction factoids

Reward threshold — or the amount of substance needed to get a “high” — increases over time. Addicts need more and more. Eventually, many don’t get a “high” or any pleasure at all — the addiction focuses around managing withdrawal.

Reward thresholds increase over time. Source: Kenny PJ. Reward mechanisms in obesity: New insights and future directions. Neuron. 2011;69:664-679.

The earlier we start eating hyperpalatable foods, the more likely we are to get hooked on them. This means that good childhood nutrition is very important — and processed foods targeted at children are a major potential health problem.

In related factoids, the longer we’re exposed to innately desirable foods, the more difficult they are to resist.  Self-control is a limited resource. So, if you struggle with being near certain foods, get away from them — fast. Get them out of your house, and move yourself away from them. Don’t torture or tempt yourself with physical proximity.

Those who prefer to binge on sweet foods tend to binge more frequently than folks who prefer to binge on fatty or salty foods.

Addicts often have higher levels of dopamine circulating in their brains than non-addicts. It’s not clear whether that’s a cause or consequence of eating.

Binge eating (independent of body weight), rather than weight, is more closely associated with addictive eating patterns. In other words, behaviour predicts addiction better than body size, weight, or fatness.

Some data indicate that compared to women, men are more likely to overeat once they begin, and are more likely to eat more than their body needs.

Philosophical musings

In the U.S., many self-destructive compulsions are considered normal. This means it’s harder to identify problem behaviours as addictions or dependencies. Indeed, if someone were to design a society ideal for food addiction – North America would probably be it.

If we quit eating a certain food – are we addicted to abstaining?

Buddhist teachings have long stated that attachment is the root of all suffering. Could this — along with mindfulness training and learning to “be present” with discomfort — be the key to unlocking addiction?

Further resources

What’s harder to kick – food or chemicals? 

Substance related disorders

Food Addiction Summit

Food Addicts Anonymous

For more on appetite and addiction, see here:

All About Appetite – Part 1

All About Appetite – Part 2

Research Roundup: Food Addiction

Is Food Addiction Real?

Kessler, David. The End of Overeating.  2009.  Rodale.

Barnard N & Stepaniak J.  Breaking the Food Seduction.  2003.  St. Martins.

References

Velez-Mitchell.  Addict Nation.  2011.  Health Communications, Inc.

Finlayson G, et al.  The Regulation of Food Intake in Humans.  http://www.endotext.org/obesity/obesity7.3/obesity7-3.html

Cohen DA.  Neurophysiological pathways to obesity: Below awareness and beyond individual control.  Diabetes 2008;57:1768-1773.

Milkman KL, Rogers T, Bazerman MH.  Harnessing our inner angels and demons: What we have learned about want/should conflicts and how that knowledge can help us reduce short-sighted decision making.  Perspectives on Psychological Science 2008;3:324-338.

Five Techniques for Avoiding Short-Sighted Decision-Making. PsyBlog. http://www.spring.org.uk/2011/06/five-techniques-for-avoiding-short-sighted-decision-making.php
Committee on Assessing Interactions Among Social, Behavioral, and Genetic Factors in Health, Lyla M. Hernandez and Dan G. Blazer, Editors.  Genes, Behavior, and the Social Environment: Moving beyond the nature/nurture debate.  2006.  National Academy of Sciences.  http://www.nap.edu/catalog.php?record_id=11693

Kessler DA.  The End of Overeating.  2009.  Rodale.

Barnard N.  Breaking the Food Seduction.  2003.  St. Martins.

Szalavitz M.  Heroin vs. Haagen-Dazs: What food addiction looks like in the brain.  April 4, 2011.  http://healthland.time.com/2011/04/04/heroin-vs-haagen-dazs-what-food-addiction-looks-like-in-the-brain

Szalavitz M.  Hooked on addiction: From food to drugs to internet porn.  April 15, 2011.  http://healthland.time.com/2011/04/15/hooked-on-addiction-from-food-to-drugs-to-internet-porn/

Parylak SL, Koob GF, Zorrilla EP.  The dark side of food addiction.  Physiology & Behavior 2011;104:149-156.

Wenk GL.  Your brain on food.  2010.  Oxford University Press.

Obesity and food addiction summit webcasts: http://www.foodaddictionsummit.org/agenda.htm

Avena NM, Rada P, Hoebel BG.  Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake.  Neurosci Biobehav Rev 2008;32:20-39.

Gearhardt AN, et al.  Can food be addictive?  Public health and policy implications.  Addiction. 2011;106:1208-1212.

Sandor RS.  Thinking simply about addiction.  2009.  Penguin Books.

Blumenthal DM & Gold MS.  Neurobiology of food addiction.  Current Opinion in Clinical Nutrition and Metabolic Care. 2010;13:359-365.

Ifland JR, et al.  Refined food addiction: A classic substance use disorder.  Medical Hypotheses. 2009;72:518-526.

Kenny PJ.  Reward mechanisms in obesity: New insights and future directions.  Neuron. 2011;69:664-679.

Avena NM, Rada P Hoebel BG. Sugar and fat bingeing have notable differences in addictive-like behavior. J Nutr. 2009;139:623-628.

McQuillan S. Breaking the bonds of food addiction.  Psychology Today.  2004.  Penguin Group.

Kiernan J.  Why Food is Addiction is Often Deadlier Than Drinking or Drugs. The Fix.  June 23, 2011.  Accessed here: http://www.thefix.com/content/oa-vs-aa

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Menopause is when the ovaries stop releasing eggs and menstruation ends for good. A woman has officially entered menopause on the 365^th day from the date of her last menstrual period.

However, women’s transition to menopause is usually gradual and involves fluctuating hormone levels and a range of symptoms for several years.

Female hormone “operation shut down” actually begins during the late twenties, but isn’t really evident until between the ages of 35 to 45 years. This is when many women start to notice changes in their bodies, minds, and feelings. Periods become irregular, the libido tanks, and counting sheep no longer helps with sleep. And hey, did someone turn up the thermostat?

A shared yet diverse experience

While there are common symptoms that many women experience (see below), and an official definition (see above), it’s important to understand that each woman’s experience of menopause is unique.

Symptoms of menopause, perceptions of menopause, and age of onset vary widely from woman to woman, region to region and by ethnicity. This is probably due to differences in

• lifestyle
• diet
• genetic factors
• reproductive history and pregnancy (for instance, on average African women have more children and hit menopause earlier than their counterparts of African descent living in the U.S., which researchers think may be due to demographic patterns of earlier and more frequent pregnancies)
• cultural factors: each culture and social group views menopause differently, which affects how women think about their own symptoms and experiences
• social factors: women have other life challenges, changes, and demands during midlife

In the U.S., about 85% of women will have entered menopause by age 52. With the population of older folks increasing in developed countries, more women are menopausal and post-menopausal.

When is too soon?

Since there’s no specific age of onset, and women’s experiences are diverse, it’s hard to define exactly what “premature” menopause is. However, if women have low sex hormone levels and their periods check out before age 40, that’s officially considered “premature”.

We don’t yet know why premature menopause occurs; it could have an autoimmune component and has been linked to other autoimmune disorders such as thyroiditis and fibromyalgia. Chances of premature menopause also go up with smoking, ovary damage (e.g. from surgery), genetic predisposition, and exposure to xenoestrogens.

What you should know about menopause

Ovaries produce estrogen, progesterone and androgens. They are signaled to do so by FSH (follicle stimulating hormone) and LH (luteinizing hormone) from the brain. With menopause, these hormones gradually decrease.

Changes in estrogen and progesterone during the life cycle

With advancing age, muscle mass and bone mass can decrease, which can influence other hormones in the body, leading to a decrease in GH, IGF-1, and DHEA.

As hormone levels change, so does the body. A perimenopausal woman should be on the lookout for:

• Loss of the menstrual cycle
• Hot flashes and night sweats
• Cardiovascular disease
• Osteoporosis
• Emotional changes
• Vaginal dryness/infections
• Incontinence/urinary tract infections
• Decline in sex drive
• Insomnia

Hormone production

As ovarian hormone production declines, sex hormones secreted by body fat and other organs such as the adrenal glands become more prevalent. The balance tips.

It’s important to keep your body fat in a healthy range with good nutrition and regular activity as you age. Having a lot of excess body fat puts your hormone production out of whack and creates systemic inflammation. That just makes things worse.

See All About Estrogens for more.

Hormone replacement therapy: A controversial option

Hormone replacement therapy (HRT) can offset low hormone levels in the body. Large studies have been completed that provide useful information about perimenopausal HRT, including the HERS study, the ERA study, and the Women’s Health Initiative Clinical Trial.

The Women’s Health Initiative Clinical Trial indicated that for women who are within 10 years of menopause who have taken HRT for 5 or more years, there is a 30% reduction in all cause mortality.

There are natural and synthetic options for HRT.

Natural hormones are substances identical to those produced in the body. Synthetic hormones are chemically altered so that companies can patent them, but still similar enough to the natural kind so they enter the cell and perform most of the same functions.

Only natural progesterone seems to help prevent cancers, normalize blood fats, restore sex drive and regulate sleep. Synthetic progestins can contribute to mood swings, fatigue, insomnia, bloating, weight gain, and anxiety.

Most published data on HRT relates to synthetic hormones, and many women’s health advocates have pointed out significant problems with using synthetic hormones, which are typically derived from non-human sources such as pregnant mares and not identical to the hormones already present in women’s bodies.

Based on available data, here’s how HRT — again, mostly with synthetic hormones — stands.

The American Association of Clinical Endocrinologists announced in 2008 that the benefits of HRT in women under 60 years of age outweigh the risks, and the use of HRT is supported by the ACOG and North American Menopause Society.

Note: Many of the negative HRT effects seem to occur when using combination therapy (synthetic estrogen + synthetic progestin) vs. estrogen only.

(Haas J, et al. Changes in the use of postmenopausal hormone therapy after the publication of clinical trial results. Ann Intern Med. 2004; 140:184-188.)

Why menopause is important

Most of the factors that accompany menopause are temporary, but some can be very harmful. Let’s highlight the biggies.

• Hot flashes/night sweats
• Cardiovascular disease
• Osteoporosis; decreased bone density
• Emotional changes
• Insomnia

“Power surge”: Hot flashes

Hot flashes aren’t really “harmful,” assuming they don’t harm your social life or light the bedsheets on fire. But they sure are a drag.

Some women never have hot flashes at all, probably because they are good at making estrogen from other sources like body fat and androgens.

Hot flashes usually last a few — seemingly interminable — minutes. During this time, skin temperature can actually increase by up to 8 degrees F. Core body temperature stays the same or decreases. Many women find that hot flashes are particularly bad at night.

Hot flashes often increase before menopause, peak 2-3 years after onset, and then taper off. Triggers include stress, coffee, spicy foods, alcohol, sugar, citrus fruits, high BMI, smoking, SSRIs, large meals, and intense exercise.

Soy and hot flashes

Just 25% of Japanese women experience hot flashes vs. 85% of North American women (although some researchers propose that these numbers might be skewed due to reporting bias).

Although there are probably many factors involved, such as genetics and other dietary factors such as fish/seafood consumption (which creates a higher level of omega-3 fatty acids), some think this variation is due to the consumption of soy.

Soy (and many other plant foods) contains isoflavones, a type of phytoestrogen, which are plant derived compounds that can exhibit hormonal activity. American women consume less than 3 mg of isoflavones per day, while women in Eastern Asia consume between 20 and 80 mg/day.

Consuming 50-100 mg/day of isoflavones from food seems to be a safe amount that helps to relieve hot flashes. This would be equivalent to consuming one of the following:

• 1 to 1½ cups soy milk
• 4-5 oz tempeh
• 4-5 oz tofu
• ½ cup edamame
• 3-4 tbsp miso
• ¼-1/2 cup soy nuts

However, flax meal may also be useful. One study showed that women suffering at least 14 hot flashes per week who added 4 tablespoons of flax meal per day to their diet for 6 weeks decreased daily hot flash frequency by 50%, and intensity dropped by 57%.

Some important notes:

Not all women efficiently convert phytoestrogens into a form the body can use to relieve menopausal symptoms.

Soy, like any food, can provoke hypersensitivity reactions. Some nutrition researchers note that soy can be allergenic or interfere with proper nutrient absorption and digestion.

If you are prone to thyroid and/or breast problems, as well as food intolerances, you might want to discuss eating more soy with a doc or dietitian first.

It’s best to get isoflavones from food rather than supplements. Isoflavone supplements might interfere with thyroid function and inhibit mineral absorption, so stick with whole food sources. Avoid consuming more than 150 mg of isoflavones per day.

Regular intake for 1-2 months is usually necessary to notice any effects from isoflavones.

Go with organic soy when possible.

The ACOG approves soy for relieving hot flashes.

Other options for hot flashes

Other options that might help to relieve hot flashes include:

• St. John’s wort (take caution as this herb interacts with various pharmaceuticals)
• yoga
• acupuncture
• massage
• meditation
• exercise

HRT is currently the only FDA approved treatment for hot flashes.

Options that don’t seem to help relieve hot flashes (and may cause additional problems) include:

• kava kava
• Dong quai
• evening primrose oil
• red clover
• ginseng
• black cohosh (Some cases of animal cancers have been reported, and there are 30 reports of serious liver damage with supplementation Mahady GB, et al. United States Pharmacopeia review of black cohosh case reports of hepatotoxicity. Menopause 2008;15(4 Pt. 1):628-638)
• wild yam cream (This contains progesterone precursors; yet humans lack the enzyme necessary to metabolize them. The only way to get true progesterone cream is with a prescription. OTC creams are fraudulent.)

Some menopause specialists simply recommend that rather than trying to eliminate hot flashes entirely, women integrate hot flashes into their daily lives: dress in layers, pop out for some fresh cool air if possible, etc.

Cardiovascular disease

Cardiovascular disease is the leading cause of death in postmenopausal women. Along with declining estradiol, as women age and put on body fat, they can develop insulin resistance/metabolic syndrome, which leads to Type 2 diabetes and further elevates their CVD risk.

While naturally occurring estradiol is cardioprotective, synthetic estrogen in HRT can lead to inflammation, blood clots, and be of no help to existing plaque on vessel walls.

To greatly decrease chances of developing heart disease as you enter menopause, do the following:

• Keep blood pressure below 120/80 mmHg
• Keep total cholesterol below 200 mg/dl
• Keep LDL below 70 mg/dl
• Keep HDL above 60 mg/dl
• Don’t smoke
• Manage stress and meditate
• Keep your body fat in a healthy range; don’t yo-yo diet
• Exercise at least 5 hours each week
• Consume plenty of whole, plant foods like vegetables, fruits, beans, whole grains, nuts and seeds
• Avoid processed foods and added sugar
• Include smaller amounts of alcohol, meat, fish, dairy, and eggs
• Drink tea and water

Osteoporosis

At menopause, calcium absorption is generally 50% below the adolescent peak rate. This is likely due to a lack of vitamin D (less time in sun, less consumed in diet, less uptake in gut).

Estrogen helps to slow bone breakdown and prevent factures by turning on vitamin D receptors in the gut (see more here: All About Vitamin D). HRT won’t help to build or replace bone, but it may help to prevent bone loss.

Ways to preserve bone mass upon menopause:

• Incorporate green leafy veggies, legumes and nuts/seeds – these seem to be the optimal sources of bone building calcium
• Get adequate sunlight to attain vitamin D (see more here: All About Vitamin D) — and hey, fresh air and exercise help relieve hot flashes too! Win-win!
• Avoid excessive alcohol, salt, carbonated drinks, and caffeine
• Check your calcium supplementation – it might contribute to the progression of cardiovascular disease. It’s best to only supplement when you can’t get enough calcium from food and vitamin D status is adequate. In addition, many women eating standard Western diets are actually deficient in magnesium and other trace minerals (such as phosphorus), not calcium.
• Eat soy – soy can increase intestinal calcium absorption and protect bone cells
• Do weight bearing exercise (resistance training, walking, etc.)
• Don’t smoke
• Include foods from the allium family – these can protect bones and inhibit cancer development
• Avoid refined sugars/grains – these don’t provide nutrients, can diminish bone health, increase inflammation, and result in mood swings and fatigue

Recent research suggests that osteoporosis is less a disease of “not enough calcium” and more about systemic inflammation and poor mineral absorption, particularly from a diet high in grains and dairy and low in veggies. (See All About Dietary Acids and Bases). There is evidence that estrogen may affect inflammatory cytokines (cell signaling molecules).

Emotional changes

Many women notice emotional highs and lows. This is a scientifically detached and polite way of saying that many women sometimes feel like they’re going nuts.

Emotional symptoms can include:

• crying spells; sadness
• irritability and anger
• panic and anxiety; sense of dread or impending doom
• depression and lethargy

To ensure a stable mood:

• Incorporate plenty of whole foods rich in vitamin C like bell peppers, citrus fruits, broccoli, teas, potatoes, and yams
• Eat foods with B vitamins for the nervous system like wild rice, brown rice, quinoa, buckwheat, polenta, and green leafy vegetables
• Get outdoors for recreation
• Eat whole grains to bump up serotonin
• Eat regular meals
• Limit processed foods, added sugars, alcohol and caffeine
• Incorporate omega-3 fats from algae, flax, hemp, chia, and walnuts
• Address underlying factors, e.g. stress, relationship difficulties, etc.

Many women find that counselling is helpful during this period. Midlife is also a period of life change, and mood changes can reflect “real” changes, shifts in priorities or life demands, and/or underlying issues (such as changes in family dynamics or caregiving).

Recognize that these symptoms are common, and (in part) related to hormonal changes — you’re not going crazy!

Insomnia

This is often due to night sweats and/or anxiety, but generalized hormone fluctuations can cause sleep disturbances too. Along with changes in sex hormones, women may notice changes in other hormones such as thyroid and/or adrenal hormones.

To promote restful sleep:

• Limit alcohol (see here for more on this: All About Alcohol) – remember that alcohol can compromise liver function, diminishing its ability to metabolize estrogens
• Limit caffeine
• Try a small serving of starchy carbohydrates in the evening, which can increase serotonin
• Avoid protein, sugar, fat, beans, and liquids before sleeping
• Melatonin or valerian might help with sleep, but side effects can occur
• Basic sleep hygiene is in order; see All About Sleep for more
• Other hormonal conditions can affect sleep, so discuss any symptoms with your doctor or endocrinologist

There are social factors too. Many midlife women are struggling with competing responsibilities: paid work, unpaid work (e.g. domestic work), caregiving for children and aging parents, etc. It’s no wonder that many of them can’t sleep!

Other physical and mental changes

Hey, where did that spare tire come from? Why are you feeling more like an apple than a pear these days? Why doesn’t food X agree with you any more? Why is it so hard to lose fat? Why are you suddenly attracted to elastic waistbands? And where did you leave your freaking car keys??!

There are many other physical and mental changes that can occur in midlife, which again reflect changes in both the physical environment (i.e. hormonal changes) and changes in your personal life (e.g. caregiving stress). This includes:

• changes in sex drive
• vaginal dryness; yeast infections; bladder infections and interstitial cystitis
• changes in breast size (as estrogen declines) and comfort (e.g. tenderness, lumpiness)
• forgetfulness; “brain fog”; difficulty concentrating
• digestive changes; new food intolerances
• water retention; bloating
• increased intensity of PMS symptoms
• difficulty losing fat
• changes in appetite and/or food cravings
• dizziness; lightheadedness
• heart palpitations
• “inner tremor” or jitteriness; some women talk about it feeling like an “inside earthquake”
• headaches; migraines
• joint pain
• tingling, “electric shock” type pain in extremities
• fatigue; lethargy
• hair loss; thinning hair
• brittle nails

Summary and recommendations

Physical, intellectual, and emotional changes in midlife are normal for men and women. Changes take a variety of forms.

Each woman’s experience of menopause is unique. You can significantly affect your menopause symptoms with good nutrition and regular activity.

Symptoms are complex and inter-related. For instance, changes in digestion or the hormonal environment can affect fat loss. Insomnia can add to your stress, worsen your mood, and make you want to reach for that caffeine.

Build a strong support network that includes health care providers, coaches, counsellors, other women, family and friends, etc. Ask for help. Don’t go it alone.

Do your homework and learn about your experiences, as well as those of other women. Chances are, you’re not “abnormal”.

If menopausal symptoms are manageable, exploring natural options is likely the best option. For those with significant and debilitating menopausal symptoms, and under the age of 60, HRT might be something to consider.

Living, exercising, and eating the PN-style way can help control symptoms and decrease chances of potential diseases associated with menopause. This includes:

• Keep your body fat in a healthy range; don’t yo-yo diet
• Exercise at least 5 hours each week, and include weight-bearing activities as well as stress-relieving activities such as outdoor walking
• Consume plenty of whole, plant foods like vegetables, fruits, beans, whole grains, nuts and seeds
• Include controlled amounts of alcohol, caffeine, meat, fish, dairy, and eggs
• Avoid processed foods, added salt, smoking, and added sugar
• Drink tea and water
• Consider eating small amounts of whole soy foods each day
• Manage stress and meditate

Extra credit

A hysterectomy will cause menstrual periods to stop, but it won’t induce menopause, because the ovaries continue to function.

Bloating with menopause/post-menopause can be due to changes in digestive abilities. Stomach acid tends to decrease. This can be alleviated with a digestive enzyme supplement, digestion tea with peppermint/ginger, limiting animal foods, using a probiotic rich food or supplement, and lightly cooking raw vegetables.

Taking a contraceptive pharmaceutical can mask perimenopuase by controlling typical symptoms. This doesn’t “change” the time of menopause for you.

Estradiol tends to suppress appetite.

The Japanese have no word for “hot flash.”

A plant-based diet is associated with fewer hot flashes.

Changes in estrogen might influence fat cell activity in the abdomen.

Men can experience hot flashes when testosterone suddenly drops, such as in prostate cancer treatment.

Current data provides assurance that isoflavone exposure at levels consistent with historical Asian soy intake doesn’t seem to result in adverse effects on breast tissue.

Cruciferous vegetables may guard against estrogen dependent cancers.

Seaweed has minerals for thyroid function and can inhibit cancer development.

Further resources

North American Menopause Society

The American Congress of Obstetricians and Gynecologists

References

Avis, Nancy, et al. Is there a menopausal syndrome? Menopausal status and symptoms across racial/ethnic groups.
Social Science and Medicine (February 2001), 52 (3), pg. 345-356.

Pinkerton JV, Stovall DW, Kightlinger RS. Advances in the treatment of menopausal symptoms. Womens Health 2009;5:361-384.

Maltais ML, Desroches J, Dionne IJ. Changes in muscle mass and strength after menopause. J Musculoskelet Neuronal Interact 2009;9:186-197.

Taylor N. Natural Menopause Remedies. New American Library. New York, NY. 2009.

Herrington DM, et al. Effects of estrogen replacement on the progression of coronary-artery atherosclerosis. N Engl J Med 2000;343:522-529.

Lakoski SG, et al. Hormone therapy, C-reactive protein, and progression of atherosclerosis: data from the Estrogen Replacement on Progression of Coronary Artery Atherosclerosis (ERA) trial. Am Heart J 2005;150:907-911.

Abdali K, et al. Effect of St. John’s wort on severity, frequency, and duration of hot flashes in premenopausal, perimenopausal and postmenopausal women: a randomized, double-blind, placebo-controlled study. Menopause 2010;17:326-331.

Bolland MJ, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ 2010;341:c3691.

Mundy, Gregory. Osteoporosis and inflammation. Nutrition Reviews 65 no.12 (December 2007): S147–S151.

Crawford AM. The Natural Menopause Handbook. Crossing Press. Berkeley, CA. 2009.

Glenville M. Healthy eating during menopause. National Book Network. Lanham, MD. 2004.

Cheung T. The all-natural menopause diet. Pegasus Books. New York, NY. 2008.

Thacker HL. The Cleveland Clinic Guide To Menopause. Kaplan Publishing. New York, NY. 2009.

Seaman B & Eldridge L. The no-nonsense guide to menopause. Simon & Schuster. New York, NY. 2008.

Messina MJ & Wood CE. Soy isoflavones, estrogen therapy, and breast cancer risk: analysis and commentary. Nutr J 2008;7:17-29.

Edelman JS. Menopause Matters. The Johns Hopkins University Press. Baltimore, MD. 2010.

Saxena T, et al. Menopausal Hormone Therapy and Subsequent Risk of Specific Invasive Breast Cancer Subtypes in the California Teachers Study. Cancer Epidemiol Biomarkers Prev. 2010;Online First.

Cassidy A. Diet and menopausal health. Nursing Standard. 2005;19:44-52.

Pines A & Berry EM. Exercise in the menopause – an update. Climacteric 2007;10(Suppl2):42-46.

Kronenberg, F. Menopausal hot flashes: A review of physiology and biosociocultural perspective on methods of assessment. J Nutr 2010;140:1380S-1385S.

Messina M. A brief historical overview of the past two decades of soy and isoflavone research. J Nutr 2010;140:1350S-1354S.

Hagey AR & Warren MP. Role of exercise and nutrition in menopause. Clin Obstet Gynecol 2008;51:627-641.

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We store fat in adipose tissue in our bodies — mostly under the skin (subcutaneous) or in the body cavity (visceral), with a small amount in our muscles (intramuscular). Body fat is an energy storage depot.

When the substances providing energy become sparse in your bloodstream, the body detects this and calls on fat reserves for backup.

Fat storage and energy

Fats are stored as triglycerides in fat cells and are released via the activity of an enzyme known as hormone-sensitive lipase (HSL). This allows fatty acids to enter the blood, where they circulate bound to a protein called albumin and enter muscles to be “burned.” “Burning” of fat is also known as beta-oxidation.

Tissues can break down fatty acids by way of this beta-oxidation. The process of beta-oxidation ultimately produces ATP, which is the energy source for cells. This takes place in the mitochondria. Fatty acids enter the mitochondria via carnitine.

When high amounts of fatty acids are being broken down and flood the mitochondria (as in starvation), there may be no immediate need for them. In this case, they form energy-rich fragments known as ketones. This is important, as fat cannot be converted into glucose, but it can provide fuel for the muscle and brain in the form of these ketones.

ATP produced from the breakdown of fat is used for metabolic processes in the body including breathing, body temperature regulation, digestion, and excretion. At rest and very low intensity exercise, we get approximately 70% of the ATP produced from fats.

Why is fat loss so important?

We need to lose fat…

As a group, people in most industrialized societies are likely to be over-fat.

This isn’t just a cosmetic problem. Excess body fat can negatively affect nearly every facet of life, including:

• decreased mobility
• poorer emotional health and self-esteem
• increased risk of organ failure
• poorer circulatory health
• increased risk of heart disease
• increased risk of stress fractures
• increased risk of strokes
• increased risk of cancers
• decreased sexual and reproductive health

Fat cells can act as endocrine factories and produce hormones that influence numerous processes in the body — most of which lead to more fat accumulation.

Beyond the health of it all, carrying a lower body fat is often considered more attractive and desirable as the underlying musculature is revealed.

Further, carrying a lower body fat is advantageous for many sport competitors (barring sumo wrestlers, linemen, etc) as extra fat weight adds drag and additional resistance that must be overcome.

Bottom line: Carrying a lot of excessive body fat makes health, body composition, and athletic performance worse.

…but it’s hard.

But here’s the problem — collectively, we’re not very good at losing fat either.

Even modern advancements in obesity treatment (e.g., bariatric surgery, medication, etc) have a success rate of less than 10% for permanent weight reduction/management.

About 95% of those who are overweight go on repeated diets, only to gain most or all of the weight back within one year. Nearly 70% of the United States is overweight or obese. The percentage of 12 to 17 year olds who are overweight has doubled since 1980.

We need a better solution. Knowing how fat loss works may be helpful.

What you should know

Fat cells are a major storage site for body fat, and are in a continuous state of turnover. Fat metabolism is regulated independently by nutritional, metabolic, and hormonal factors; the net effect determines levels of circulating fatty acids and the extent of body fat.

Fat loss and hormones

Fatty acid release and use requires lower insulin levels and an increase of the hormones glucagon, cortisol, epinephrine, and growth hormone. These “anti-insulin” hormones activate HSL. The other major hormone that influences fat metabolism is thyroxine (thyroid hormone).

After a large feeding, glycogen is synthesized until stores are replenished. If high blood sugar persists, glucose is converted to fatty acids. Amino acids can also be converted to fatty acids. The enzyme necessary for cells to accept triglycerides is lipoprotein lipase.

In the un-fed state, insulin concentrations fall, and the anti-insulin hormones increase. This accelerates fat use.

Fat loss and caloric deficit

When we decrease our caloric intake significantly, the body preserves fat stores very efficiently. Since insulin is low, thyroid hormone production is decreased. With this, resting metabolism is lowered. This can take place within 24 hours of starting an extreme diet.

The body’s response to calorie deprivation makes rebound weight gain all but definite once the diet is discarded. Muscle is usually lost, so the body usually becomes fatter.

Fats are more than just a fuel source during rest and lower intensity exercise. Fats restore phosphagens that have been exhausted during high intensity exercise. After intense exercise sessions, oxygen uptake is increased, which allows restoration to pre-exercise conditions (the “afterburn” effect).

Stages of fuel use during fasting

Fat loss is a complex problem

With our focus on specific nutrients, intense nutrition counseling, dieting and processed food consumption over the past 30 years, body fat levels have also increased. In other words, more information, more dieting, more junk food has given us more fat.

While some of this may seem counter-intuitive, it illustrates the importance of body awareness (hunger/satiety cues), avoidance of processed foods, regular physical activity and influential food advertising.

Summary and recommendations

To maintain a low body fat and/or lower body fat:

• Exercise at least 5 hours per week
• Eat whole/unprocessed foods at regular intervals, while being aware of physical hunger/fullness cues
• Sleep 7-9 hours per night
• Don’t engage in extreme diets
• Stay consistent with your habits
• Incorporate non-exercise physical activity
• Ignore food advertising

For extra credit

Aspartame was approved for use in 1981, and while this non-caloric sweetener was hypothesized to help control body weight, since 1980, levels of body fat have increased.

Factors associated with lower levels of body fat include:

• nuts
• green tea
• low energy-density foods
• dietary protein
• avoiding refined carbohydrates
• adequate hydration
• dietary fibre
• fruits and vegetables
• regular exercise
• adequate sleep
• a supportive social network

While cortisol can break down muscle tissue, it can also break down body fat.

If you increase physical activity and nutritious food intake, metabolism will increase.

Blaming weight gain on calories is like blaming wars on guns. The diet is not the cause of excessive body fat levels. Rather, it’s the entire lifestyle.

Severe calorie deprivation inhibits the production of serotonin, a brain chemical needed to control appetite and maintain harmony with food.

Further reading

CLA & Bodyfat

Good body fat?

Gaining body fat with exercise

4 reasons you’re not losing fat

Sex differences in fat loss

Abdominal fat and your fate

References

Potenza MV & Mechanick JI. The metabolic syndrome: definition, global impact, and pathophysiology. Nutr Clin Pract 2009;24:560-577.

Borer KT. Exercise Endocrinology. Human Kinetics. Champaign, IL. 2003.

Mahan LK & Escott-Stump S. Eds. Krause’s Food, Nutrition, & Diet Therapy. 11th ed. Saunders Publishing, Philadelphia, PA. 2004.

Murray RK, Granner DK, Mayes PA, Rodwell VW, eds. Harper’s Illustrated Biochemistry. 26th ed. McGraw Hill. 2003.

Barnard ND, et al. Nutrition Guide for Clinicians. 1st ed. PCRM. 2007.

Howley ET & Franks BD, eds. Health Fitness Instructor’s Handbook, 4th ed. Human Kinetics. Champaign, IL. 2003.

Bullo M, et al. Inflammation, obesity and comorbidities: the role of diet. Public Health Nutr 2007;10:1164-1172.

Garcia OP, et al. Impact of micronutrient deficiencies on obesity. Nutr Rev 2009;67:559-572.

Anderson AS & Caswell S. Obesity management – an opportunity for cancer prevention. Surgeon 2009;7:282-285.

Dennis EA, et al. Beverage consumption and adults weight management: A review. Eat Behav 2009;10:237-246.

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The thyroid gland is found in the neck, right below the voice box (larynx). It’s made of two large lobes that are connected in the middle. In an adult, the thyroid usually weighs about 1 ounce.

The thyroid is filled with cells that contain protein-iodine complexes. These complexes are precursors of thyroid hormones.

Thyroid hormones

Although they’re often referred to as “thyroid hormone”, singular, the thyroid gland produces two hormones: triiodothyronine (T3) and thyroxine (T4). These hormones play a vital role in regulating growth and metabolism.

The hypothalamus releases TRH (thyrotropin releasing hormone), which stimulates the release of TSH (thyroid stimulating hormone) from the pituitary gland. TSH makes its way to the thyroid and promotes its growth and development. The release of T3 and T4 is controlled by TSH.

Thyroid gland feedback loop

Once T3 and T4 are released from the thyroid, they attach to proteins (mainly TBG and albumin) and move through the bloodstream.

The thyroid gland releases about 20 times more T4 than T3. But T3 is more potent than T4. Once T4 enters target tissues, it is converted to T3.

When T3 and T4 arrive at a target cell, they detach from the carrier protein and work their magic. Thyroid hormones are then degraded in target cells and the liver.

Molecular structures of T3 and T4

Why is the thyroid so important?

The thyroid is one of the “master controllers” that regulates nearly every major metabolic function in the body.

Thyroid hormones regulate the metabolic rate of all cells, as well as the processes of cell growth, tissue differentiation, and reproductive function. Thyroid hormones can potentially interact with any cell in the body.

Thyroid hormones are necessary for (and promote) protein anabolism when ample carbohydrates and fats are available. When the amount of thyroid hormones is excessive or when energy from food is deficient, T3 and T4 may then promote protein breakdown.

What you should know

Hormone status can influence metabolic rate, particularly in those with endocrine disorders such as hyperthyroidism and hypothyroidism. It’s also possible for one disorder to shift into another — for instance, hyperthyroid can become hypothyroid. Thyroid disorders are most often autoimmune, although they can have other causes.

Hyperthyroidism

In hyperthyroidism, or over-active thyroid function, it’s as if your body’s “motor” is revving at high speed. Symptoms can include:

• racing heart and palpitations
• trouble sleeping
• tremor and nervousness
• weight loss
• hair loss
• muscle aches and weakness
• diarrhea and over-active digestive system
• sweating and trouble tolerating heat
• exophthalmos (bulging eyes)

Hypothyroidism

Hypothyroidism refers to low thyroid function — the opposite of the above. The “motor” slows down.

If you’re struggling to lose fat even with a solid nutrition plan and regular, intense exercise, and you have some or all of the symptoms below, consider hypothyroidism as a possible contributor, especially if you’re female.

Indeed, 1 in 8 women will develop a thyroid problem at some point in life. Unexplained weight gain is one symptom of hypothyroid, but others include:

• tiredness, fatigue, lethargy
• depression and losing interest in normal activities
• forgetfulness
• dry hair and skin
• puffy face
• slow heart rate
• intolerance to cold
• constipation
• brittle nails
• muscle cramping
• changes in menstrual cycle

Women may also develop a temporary thyroid inflammation after pregnancy.

Screening for thyroid function

Some organizations recommend that any person over the age of 40 be screened periodically for thyroid function. This can be done with a blood test measuring TSH.

As previously mentioned, TSH stimulates the thyroid. If the thyroid does not respond, then TSH levels will rise. Overly high TSH levels mean that the signal is being released, but the thyroid isn’t listening. (Imagine screaming louder and louder at a person who can’t hear well.)

TSH reference ranges (may be different if on thyroid replacement): 0.4 – 4.0 mIU/L

If diagnosed, hypothyroidism is controlled with thyroid hormone replacement (specific to the individual). Many people assume that correcting the thyroid imbalance will result in a miraculous decrease of body fat – but the changes are usually subtle and take time. Nutrition, exercise and lifestyle issues all need to be addressed.

The role of iodine

As you might guess from the “iodo” in T3 and T4′s full names, we need dietary iodine to synthesize thyroid hormones. To meet the body’s demand for thyroid hormones, the thyroid gland traps iodine from the blood and uses it for the synthesis of T3 and T4.

Iodine deficiency results in a lower production of T4. The body normally contains 20 to 30 mg of iodine, with more than 75% in the thyroid gland. The RDA for iodine is 150 mcg/day for adult men and women. Diets that exclude iodized salt, fish, and seaweed have been found to contain very little iodine. Iodine from seaweed appears to enhance thyroid function.

Goitrogens and soy

A goiter is a mass of tissue in the thyroid gland. Left untreated, this can become extremely large.

A goiter

Substances that contribute to this are known as “goitrogens”.

Goitrogens, which exist naturally in foods, can cause goiter by blocking the uptake of iodine from the blood by the thyroid. Goitrogens are inactivated by heating or cooking. Most goitrogens are not of clinical importance unless they are consumed in large amounts or there is coexisting iodine deficiency.

Some evidence suggests that soy acts as a goitrogen. Soy intake in controlled amounts, from unprocessed foods, doesn’t seem to negatively impact thyroid function; the effects of large amounts of processed soy are less clear. If using a synthetic thyroid medication, notify your doctor of soy food intake.

Summary and recommendations

• Consume adequate iodine
• Don’t drastically restrict calories
• Consume adequate carbohydrates and fats
• Maintain a 5 hour per week exercise regimen
• If symptoms of hypothyroidism are suspected, request a TSH test from your physician
• Get 7-9 hours of sleep each night
• Avoid synthetic chemicals found in conventional food items, body products and food containers when possible

For extra credit

Recent findings also indicate that smoking tobacco may be associated with an increased risk of goiter in iodine-deficient areas.

Hyposecretion of thyroid hormone during years of growth can lead to cretinism. This is characterized by low metabolic rate, poor growth status, and even mental retardation.

Nervous system stimulation increases thyroid hormone release and is associated with increased food intake and weight gain.

Basal metabolism, which accounts for up to 65% of daily metabolism, decreases in starvation because of reduced thyroid hormone secretion (among other things).

T3 and T4, at higher concentrations, increase the number of beta-adrenergic receptors and augment the fat and carbohydrate metabolizing actions of catecholamines.

Avoiding some chemicals found in pesticides, herbicides, eating containers (e.g., plastics), and body products (e.g., lotion, shampoo) may help to preserve thyroid function (Chemicals that contribute to thyroid dysfunction)

Further reading

T2 – The Fat Terminator?

All About Energy Balance

Thermogenesis

References

Mahan LK & Escott-Stump S. Eds. Krause’s Food, Nutrition, & Diet Therapy. 11th ed. Saunders Publishing, Philadelphia, PA. 2004.

Borer KT. Exercise Endocrinology. Human Kinetics. Champaign, IL. 2003.

Beers MH, Berkow R eds. Merck Manual. 17th ed. Merck Research Laboratories. Whitehouse Station, NJ. 1999.

An Evidence-Based Approach to Vitamins and Minerals. Jane Higdon. The Linus Pauling Institute. 2003.

Teas J, et al. Seaweed and soy: companion foods in Asian cuisine and their effects on thyroid function in American women. J Med Food 2007;10:90-100.

Dillingham BL, et al. Soy protein isolates of varied isoflavone content do not influence serum thyroid hormones in healthy young men. Thyroid 2007;17:131-137.

Messina M & Redmond G. Effects of soy protein and soybean isoflavones on thyroid function in healthy adults and hypothyroid patients: a review of the relevant literature. Thyroid 2006;16:249-258.

Boas M, et al. Environmental chemicals and thyroid function: an update. Curr Opin Endocrinol Diabetes Obes 2009;16:385-391.

Triggiani V, et al. Role of iodine, selenium, and other micronutrients in thyroid function and disorders. Endocr Metab Immune Disord Drug Targets 2009;9:277-294.

Miller MD, et al. Thyroid-disrupting chemicals: interpreting upstream biomarkers of adverse outcomes. Environ Health Perspect 2009;117:1033-1041.

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Growth hormone (GH), also known as somatotropin, is an anabolic hormone made and secreted by the pituitary gland.

GH is a large polypeptide thought to encourage growth indirectly by stimulating the release of growth factors from the liver and muscle (e.g., IGF-1).

These growth factors create the cascade of events typically associated with higher GH concentrations. GH is released in response to growth hormone releasing hormone (GHRH) produced by the hypothalamus.

Why is growth hormone so important?

GH helps bone, muscle, and other tissues grow.

In the muscle, GH stimulates protein synthesis as well as fat metabolism. GH recruits fatty acids from storage and tells the body to use fatty acids for energy.

Interestingly, as GH limits the storage of fats and mobilizes them for energy, blood sugar levels concurrently increase. In this way, GH “spares” carbohydrates from breakdown, and the level of sugar in the blood increases. This is why long-term GH replacement may predispose one to insulin resistance.

The effects of GH on fat mobilization can begin at 20 minutes after release and last up to 3 hours.

You may wonder why intense exercise is so effective at helping you lose fat, even though it doesn’t seem like a few sets of heavy squats would burn that many calories. Many researchers credit the concomitant appearance of high concentrations of plasma fatty acids and GH that follow intense training.

GH also

• Decreases blood sugar utilization
• Decreases glycogen synthesis
• Increases amino acid transport into cells and protein synthesis
• Increases fat breakdown and utilization
• Increases collagen synthesis and cartilage growth
• Increases retention of nitrogen, sodium, potassium, and phosphorus
• Increases kidney flow and filtration
• Enhances immune function

What you should know

The reference range for healthy GH levels is 0.06 – 8.0 ng/mL.

When someone is GH deficient, GH replacement seems to be safe and may even promote health – at least with long-term monitoring by a physician. There seems to be a mild risk of insulin resistance.

Sleep and GH

Sleep is associated with the release of hormones such as GH. This may be why sleep helps us repair and recover. Sleep associated GH secretion has also been linked to the nocturnal rise in fatty acid release.

As one ages, there is a decrease in sleep duration and GH secretion. Sleep deprivation in young individuals reduces GH secretion and may contribute to premature development of the metabolic syndrome. As you can see in the diagram below, GH secretion peaks late at night.

Exercise and GH

The secretion of GH during and after exercise is proportional to intensity. The tougher and harder the exercise, the more GH is released. Think sprints instead of long slow distance runs.

Increases in GH secretion are related to increases in acids, by-products of high intensity exercise. Also, catecholamines may stimulate GH secretion. Rest periods of 60 seconds or less can help stimulate GH release.

GH slowly rises during an intense workout, but it actually peaks only when the workout is over. Thus, the peak GH release concurs with the maximal fatty acid release from fat tissue. Exercise also appears to increase the amplitude and number of GH pulses during the day.

Reducing calorie intake doesn’t seem to create a GH deficit. Data indicate that cutting calorie intake by 25% doesn’t significantly reduce GH levels, and people who exercise with the right type of training may actually see GH increase.

Summary and recommendations

To ensure healthy growth hormone levels:

• Exercise intensely, using many muscle groups
• Exercise with multiple sets, short rest periods (<60 seconds) and heavy weight (~10 rep max)
• Ensure adequate carbohydrate and protein consumption before and after workouts
• Avoid/limit alcohol consumption
• Get 7-9 hours of sleep each night
• Maintain a lean/healthy body composition

Further resources

All About Sleep

Minutemen

The Fountain Of GH

For extra credit

GH and insulin function as antagonists – GH is hyperglycemic and insulin is hypoglycemic.

Psychological stress that elicits anxiety, fear, or anger can induce secretion of GH.

After exercise, neutrophil concentrations increase for several hours, most likely in response to delayed GH surge; this may enhance immune function.

Menstrual cycle has little effect on the secretion of GH during exercise; however, higher levels of GH may be noticed while at rest. One of the reasons females mobilize more fatty acids during exercise is due to greater blood concentrations of GH.

Excessive secretion of GH throughout the “growth years” results in an irregular pace of skeletal growth. This is known as gigantism. Excessive secretion of GH after the “growth years” can result in acromegaly. Abnormally low secretion of GH throughout the “growth years” may cause dwarfism.

GH is structurally similar to the placental hormone human chorionic somatomammotropin (AKA human placental lactogen).

Excess body fat can decrease GH output.

Alcohol consumption can decrease GH secretion.

Carbohydrate and protein intake before and after exercise sessions can enhance GH response.

Decreased secretion of GH occurs with overtraining. This appears to be due to impaired hypothalamic function.

GH increases the formation of hydroxyproline from proline and boosts cartilage synthesis.

References

Borer KT. Exercise Endocrinology. Human Kinetics. Champaign, IL. 2003.

Harvey RA, Champe PC eds. Pharmacology 2nd ed. Lippincott Williams & Wilkins. 2000.

de Salles BF, et al. Rest interval between sets in strength training. Sports Med 2009;29:765-777.

Redman LM, et al. The effect of caloric restriction interventions on growth hormone secretion in non-obese men and women. Aging Cell 2009;Oct 30 Epub.

Svensson J & Bengtsson BA. Safety aspects of GH replacement. Eur J Endocrinol 2009;161 Suppl 1:S65-S74.

Schuster DP. Changes in physiology with increasing fat mass. Semin Pediatr Surg 2009;18:126-135.

Kraemer WJ & Ratamess NA. Hormonal responses and adaptations to resistance exercise and training. Sports Med 2005;35:339-361.

Godfrey RJ, et al. The exercise-induced growth hormone response in athletes. Sports Med 2003;33:599-613.

Goto K, et al. Prior endurance exercise attenuates growth hormone response to subsequent resistance exercise. Eur J Appl Physiol 2005;94:333-338.

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Ever wonder what makes you hungry? Why some foods look more appealing than others? Why you’re always hungry for dessert? Or why you might open the fridge full of food, then stand there and say, “We have nothing good to eat!”?

The body is not a simple container of calories that can be added and subtracted. We’re driven by a complex play of chemicals that orchestrate food intake, desire, and food associations.

Appetite is our desire to eat.

It’s controlled by a complicated interaction of hormonal signals that originate from fat cells, cells of the pancreas and cells in the gut. These signals are also processed through cognitive and emotional filters.

For example, if you ask a North American, “What’s comfort food?” they might say “macaroni and cheese”. Pretty sure you wouldn’t get the same answer in, say, Mongolia or Rwanda. The foods we crave are a product of physiology and psychology.

Appetite is different from hunger. Hunger is our physical need to eat. You can want to eat but not need to eat (for example, wanting to eat dessert after a big meal). Or you can need to eat but not want to eat (for example, losing your interest in food when you’re stressed).

How does this all work? And who’s driving the bus?

Good luck counting calories. This shows some of the appetite regulation pathways.

For anyone who has purposefully controlled food intake to lose weight, they know how powerful counter-regulation can be. Much of this seems to be mediated, or shaped by, our neuro-endocrine system, aka the interaction between our brains and our hormones.

When we lose stored fat, our body mounts a major response to conserve energy and boost appetite, defying further weight loss and encouraging regain.

Why is appetite regulation important?

If we under- or over-eat, problems arise. We can become malnourished, obese, fail to repair, lose reproductive ability and/or develop diseases.

For those who want to decrease body fat, a conscious restriction of energy intake is generally unsuccessful (more than 90% of the time weight is regained – and then some). On the other hand, some people are successful at losing fat. Why does the first group fail and the second group succeed?

Finding the master controls

One of the best ways to grasp the importance of appetite regulation is to knock it out. In other words, the best way to learn what a hormone/gland does is to get rid of it and see what happens.

For instance, a simple defect in the hypothalamus, located in the brain, might mean someone may eat or starve themselves to death, like with Prader-Willi Syndrome. This tells us that the hypothalamus has a big role to play.

In fact, the hypothalamus is the ringmaster of appetite, but there are lots of acts in the circus. Major players in appetite regulation include insulin, thyroid hormone, glucagon like peptide-1 (GLP-1), endocannabinoids and cortisol. If any of these get out of whack, you can lose your life, literally.

We’re still learning about new pathways and chemicals involved in appetite, but below is a list of what we’ve got so far.

Orexigenic means appetite-stimulating, while anorexigenic means appetite-suppressing. (Both of these come from the Greek root orexis, or desire/appetite — notice here how “wanting to eat” is important.)

Simple, huh? Not.

From: Magni P, et al. Feeding behavior in mammals including humans. Ann NY Acad Sci 2009;1163:221-232

What you should know

Appetite is governed by two organ systems of the body, the endocrine system and the nervous system — their connection is sometimes known as the “neuroendocrine system”.

The endocrine system & appetite

Quick — what’s the largest endocrine organ in the body? You might be surprised: it’s the GI tract.

Yep, your gut is the biggest hormone player on the block. It produces and processes all kinds of hormones ranging from neurotransmitters to anabolic storage hormones to sex hormones.

The organs of the endocrine system are sensitive to changes in the body, and, in response to these changes, send out messengers (called hormones) to tell the body how to respond. These energy regulating hormones are classified into either short term or long term. The vagus nerve is the key connection between the gut and the brain.

Various hormones play a role in appetite regulation and energy balance, including:

Click to enlarge: GI hormones known to affect food intake (Source: Neary MT & Batterham RL. Gut hormones: Implications for the treatment of obesity. Pharmacology & Therapeutics 2009;124:44-56.)

The nervous system & appetite

The nervous system acts via nerve impulses and neurotransmitters (hormone-like chemicals), directing nervous tissues, smooth muscles, and other organs of the body to move, mix, and propel foodstuffs that enter the digestive system.

While some appetite control originates from nervous and hormonal connections between the digestive system and the brain, the digestive system possesses its own, localized nervous system, referred to as the enteric nervous system. It’s the “mini-brain” located in your gut. In this mini-nervous system, neurotransmitters are released, which can relay, amplify and modulate different signals between cells of the body.

Some of the neurotransmitters involved with appetite regulation include:

Other gut-brain interactions

Appetite medications

Sibutramine is the only regularly used anti-obesity medication. It acts as a norepinephrine-serotonin reuptake inhibitor. It causes hazardous side effects with only minimal impact on weight.

Rimonabant is a cannabinoid type 1 receptor antagonist. It isn’t on the market since it causes psychiatric disturbances and increased suicide risk.

And really, as of now, obesity meds don’t help at all. Patients might lose 10-15% of body weight, but 6 months later the weight is back on.

Exercise

Physical activity plays an important role in appetite regulation. Some data show that appetite responses to exercise are strongly influenced by energy balance in men, but less in women.

Those who regularly exercise become more efficient at using body fat as a fuel source, and this can help with regulating appetite (since people that don’t exercise use more carbs and blood sugar fluctuations = appetite swings).

Exercise can moderate levels of leptin, ghrelin and insulin. (See leptin cycle below.)

Also, PYY 3-36 might increase with exercise, especially with stuff like walking, jogging and biking (rather than higher intensity stuff). Moderate to intense exercise transiently suppresses appetite.

Bariatric surgery

Many of the gut hormones and neurotransmitters mentioned seem to be affected (at least temporarily) after bariatric surgical procedures. This may promote satiety, at least in the short term.

Summary and recommendations

Eating a reasonable amount of food each day to support health and regulate appetite goes beyond willpower and calorie counting.

Acknowledging the information our body relays about hunger and fullness can be helpful in regulating appetite. Only when our physiological foundation is polluted with excess stress, weight, processed foods, and/or lack of physical activity will appetite balance become defective.

The appropriate release, response and balance of gut hormones and neurotransmitters seem to depend upon a diet consisting of whole foods.

While we don’t know exactly what it takes to manage appetite, we do know the human body doesn’t have a longstanding relationship with processed food products, and they might short-circuit our appetite regulation pathways.

Social rituals of eating, such as eating while distracted (e.g. while driving or watching TV), eating too rapidly (e.g. while rushing to do errands), or always having dessert may also affect our desire to override natural hunger and fullness cues.

Extra credit

Estrogen deficiency might result in a higher energy intake and increased body weight. Food intake varies across the menstrual cycle. Women tend to eat more in the luteal phase (the premenstrual period) compared with the follicular phase.

Testosterone (directly) seems to have little effect on food intake, although many people supplementing anabolic doses of testosterone (e.g. bodybuilders) do report increased appetite.

Including a balanced intake of omega-6:omega-3 fats can help with appetite regulation.

Protein and fibre all seem to help control appetite. Refined carbohydrates, on the other hand, appear to increase appetite. Dietary fat has mixed results; when combined with refined carbohydrate it seems to increase appetite while on its own or combined with protein, it typically decreases appetite.

Elderly people have less appetite than young people from not only decreased energy expenditure but also from mechanisms potentially involving sex–steroid balance as well as altered CNS signaling to and from peripheral organs.

It’s now recognized that overfat individuals have lower blood concentrations of vitamins and minerals compared to leaner individuals. This may lead to a greater appetite and changes in fat deposition.

Further resources

The best appetite suppressant…

The end of overeating

References

Weyer C. Hormones in concert. The Scientist. http://www.the-scientist.com/2009/12/1/34/1/

Kessler D. The End Of Overeating. 2009. Rodale.

Hagobian RA & Braun B. Physical activity and hormonal regulation of appetite: sex differences and weight control. Exerc Sport Sci Rev 2010:38:25-30.

MacLean PS, et al. Regular exercise attenuates the metabolic drive to regain weight after long-term weight loss. Am J Physiol Regul Integr Comp Physiol 2009;297:R793-R802.

Conis E. Hungry after a workout? Jan 4 2010. http://www.latimes.com/features/health/la-he-snacks4-2010jan04,0,1723552.story

Carr TP, et al. Endocannabinoids, metabolic regulation, and the role of diet. Nut Res 2008;28:641-650.

Chaudhri OB, et al. Gastrointestinal satiety signals. Int J Obesity 2008;32:S28-S31.

Chaudhri OB, et al. Gastrointestinal satiety signals. Annu Rev Physiol 2008;70:239-255.

Neary MT & Batterham RL. Gut hormones: Implications for the treatment of obesity. Pharmacology & Therapeutics 2009;124:44-56.

Magni P, et al. Feeding behavior in mammals including humans. Ann NY Acad Sci 2009;1163:221-232.

Garcia OP, et al. Impact of micronutrient deficiencies on obesity. Nut Rev 2009;67:559-572.

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Testosterone molecule

Testosterone is a steroid hormone from the androgen group.

The androgens are a group of steroids that have anabolic (aka growth) and/or masculinizing effects in both males and females. Testosterone is the most important androgen in humans.

Testosterone regulates libido, energy, immune function, muscle development and bone health.

How is testosterone made?

In males, Leydig cells in the testes synthesize testosterone. In females, the ovaries and adrenal glands synthesize a much smaller amount of testosterone.

Testosterone secretion is controlled by GNRH, which is released by the hypothalamus in pulses. These pulses stimulate the pituitary gland to secrete LH. LH causes the enzymatic conversion of cholesterol into testosterone in the Leydig cells. Indeed, “cholesterol” has a bad rap in the mass media, but in fact all of our steroid hormones begin with cholesterol. (See chart below.)

Synthesis of steroid hormones. Click to enlarge.

Testosterone, like other hormones, is regulated by a feedback loop. If the body thinks there’s too much, it “turns off the tap” at the source (i.e. in the brain) or converts the excess to something else such as estradiol or DHT.

Testosterone feedback loop in men

Why is testosterone so important?

One of testosterone’s major roles is to control muscle growth.

Androgen exposure throughout early development determines the number and size of motor units. Number, size, and physiological characteristics of motor units determine the size and physiological characteristics of muscle fibres. Thus, the ability of muscle to hypertrophy (get bigger) in adulthood may be determined in part by intrauterine androgen exposure.

Exercise and testosterone

Exercise-associated increases in testosterone may amplify training-induced muscle growth.

Stimulation of beta-adrenergic receptors encourages testosterone synthesis and release in a dose dependent fashion — the more stimulation, the more synthesis. Thus, increases in plasma concentrations of testosterone are relative to the intensity of exercise. The harder you train, at least with resistance exercise or metabolic conditioning, the more testosterone you get.

Scientists think that sympathetic nerve activity and catecholamine secretion — which occur to a much greater extent during, say, a 20-rep squat set than, say, a pleasant stroll — stimulate testosterone during exercise.

However, exercise type also matters. Extended bouts of endurance exercise seem to suppress testosterone.

Sex differences in testosterone release

Moderate to high intensity exercise increases plasma concentrations of testosterone in a sex-specific fashion. In other words, intense exercise causes testosterone release, more so in men than in women.

Plasma testosterone increases occur in men after various forms of exercise, as long as that exercise is high intensity. On the other hand, women respond to intense exercise with very small and/or delayed testosterone increases, or even no testosterone increases at all.

What you should know about testosterone

Sex differences in testosterone levels

Normal serum total testosterone levels vary from person to person over time, but in general men have much more than women. Typical ranges:

Male: 230-1000 ng/dL
Female: 28-80 ng/dL

Testosterone and age

Testosterone levels increase during puberty from <20 ng/dL to around 300 – 1200 ng/dL at full maturity.

Serum testosterone is secreted in pulses and is circadian. In the second half of puberty, levels are elevated more at night than during the day. During puberty, increases in circulating testosterone and estradiol induce a 1 ½ to 3-fold amplification of pulsatile growth hormone secretion.

Conversely, testosterone levels decline as we age.

How testosterone may change with advancing age

Test-osterone

One blood sample is enough to establish circulating testosterone levels, although sometimes doctors may also test salivary testosterone, and if you’re competing in the Olympics, you may find yourself giving a urine test for androgens as well.

Since 98% of testosterone is bound to carrier proteins in the serum (sex hormone binding globulin or SHBG), alterations in these protein levels will change total testosterone levels.

SHBG is produced in the liver and its production is increased by estrogens and hyperthyroidism. SHBG is decreased by androgens, advancing age, and hypothyroidism. Thus, tests may also look for changes in SHBG.

Low testosterone

Several factors can suppress testosterone output and ultimately reproductive function. These factors include:

• chronically low calorie intake (>20% below basal needs) and chronically high calorie intake (especially if obesity results)
• low nutrient intake and vitamin/mineral deficiency
• low fat intake
• depression
• drug use
• overtraining
• limited sexual activity
• stress and anxiety
• aging
• obesity and other metabolic disorders
• overuse of hormonal contraception (in women)
• chronic illness/infection
• poor, minimal, and disrupted sleep (including sleep apnea)

Both men and women can suffer from low testosterone. Symptoms of low testosterone include:

• low energy, fatigue, and lethargy — loss of “mojo”
• decreased strength and work capacity
• low sexual desire, lack of sexual responsiveness and weaker orgasms or difficulty achieving orgasm
• loss of lean body mass, including muscle and bone density, along with an increase in body fat
• increased cardiovascular risk (including poor blood lipid profile), higher blood pressure

Supplementing testosterone

Many athletes supplement testosterone for bigger muscles and/or better athletic performance. Excessively high doses of testosterone, taken over a long period, can result in:

• acne and oilier skin
• mood changes ranging from hostility to euphoria (though evidence is mixed regarding the prevalence and details, as well as individual susceptibility)
• hair growth (in women) or hair loss
• masculinization of facial features, voice deepening (in women)
• breast growth in males as excess testosterone converts to estrogen
• testicular atrophy in males
• disruption of menstrual cycles in females; increased incidence of reproductive disorders
• certain types of muscle and connective tissue damage
• increased cardiovascular disease risk, including increased blood pressure and heart myopathies along with deep venous thrombosis and embolisms

However, endocrinologists are now starting to prescribe testosterone therapeutically, either for replacement (e.g. in older men and women) or to treat symptoms of many chronic degenerative diseases. The side effects of excessive testosterone listed above generally do not apply to therapeutic and replacement doses.

Summary and recommendations

To maximize testosterone levels for muscle growth, recovery and health:

• Engage in regular, intense exercise sessions
• Don’t severely restrict calories to more than 20% below base needs
• Make sure you are consuming enough micro- and macronutrients
• Engage in safe, regular sexual activity (yes, PN says go get some action!)
• Avoid medications/drugs
• Get adequate sleep, 7-9 hours per night
• Control stress and anxiety levels

Further resources

Male Hormones: Adjustment or Replacement

The Big T, Part 1

The Big T, Part 2

For extra credit

Testosterone facilitates spontaneous growth hormone secretion.

Sympathetic nerve stimulation increases testosterone synthesis and release.

Testosterone levels increase during the summer months.

Sexual arousal increases LH pulses (which increases testosterone levels).

Alcohol, aspirin, marijuana, codeine, lots of sugar, and opioids can decrease testosterone levels.

Diets higher in protein, cholesterol, and fat tend to maintain testosterone levels.

Eating 1-2 servings of whole, unprocessed soy foods doesn’t seem to have any negative effect on testosterone levels. However, high levels of soy intake may be a problem.

References

EndoText.org Endocrinology of Male Reproduction.

Beers MH, Berkow R eds. Merck Manual. 17th ed. Merck Research Laboratories. Whitehouse Station, NJ. 1999.

Murray RK, Granner DK, Mayes PA, Rodwell VW, eds. Harper’s Illustrated Biochemistry. 26th ed. McGraw Hill. 2003.

Borer KT. Exercise Endocrinology. Human Kinetics. Champaign, IL. 2003.

Harvey RA, Champe PC eds. Pharmacology 2nd ed. Lippincott Williams & Wilkins. 2000.

Almeida OP, et al. Low free testosterone concentration as a potentially treatable cause of depressive symptoms in older men. Arch Gen Psychiatry 2008;65:283-289.

Goh VH & Tong TY. Sleep, sex steroid hormones, sexual activities, and aging in Asian men. J Androl 2009;Aug 14 Epub.

Uchida MC, et al. Hormonal responses to different resistance exercise schemes of similar total volume. J Strength Cond Res 2009;23:2003-2008.

Hackney AC. Effects of endurance exercise on the reproductive system of men: the “exercise-hypogonadal male condition”. J Endocrinol Invest 2008;31:932-938.

Rocha JS, et al. Mild calorie restriction does not affect testosterone levels and testicular gene expression in mutant mice. Exp Biol Med (Maywood) 2007;232:1050-1063.

Traish AM, et al. The dark side of testosterone deficiency: I. Metabolic syndrome and erectile dysfunction. J Androl 2009;30:10-22.

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Insulin is a peptide hormone secreted by the pancreas in response to increases in blood sugar, usually following a meal.

However, you don’t have to eat a meal to secrete insulin. In fact, the pancreas always secretes a low level of insulin.

Insulin secretion

After a meal, the amount of insulin secreted into the blood increases as blood sugar rises. Similarly, as blood sugar falls, insulin secretion by the pancreas decreases.

Insulin thus acts as an “anabolic” or storage hormone. In fact, many have called insulin “the most anabolic hormone”. Once insulin is in the blood, it shuttles glucose (carbohydrates), amino acids, and blood fats into the cells of the body.

Insulin feedback loop – determined by blood glucose levels

If these nutrients are shuttled primarily into muscle cells, then the muscles grow and body fat is managed. If these nutrients are shuttled primarily into fat cells, then muscle mass is unchanged and body fat is increased.

Insulin’s main actions

Rapid (seconds)

• Increases transport of glucose, amino acids (among the amino acids most strongly transported are valine, leucine, isoleucine, tyrosine and phenylalanine), and potassium into insulin-sensitive cells

Intermediate (minutes)

• Stimulates protein synthesis (insulin increases the formation of new proteins)
• Activates enzymes that store glycogen
• Inhibits protein degradation

Delayed (hours)

• Increases proteins and other enzymes for fat storage

Why is insulin so important?

The pancreas releases insulin whenever we consume food. In response to insulin, cells take in sugar from the bloodstream. This ultimately lowers high blood sugar levels back to a normal range.

Like all hormones, insulin has important functions, and an optimal level.

Without enough insulin, you lose all of the anabolic effects, since there is not enough insulin to transport or store energy or nutrients. Individuals with type 1 diabetes don’t produce insulin; if left untreated, they die.

On the other hand, if blood levels of insulin are always high, we also have trouble.

Continual elevation of insulin leads to large amounts of fat gain and risk for cardiovascular disease. This can lead to the development of type 2 diabetes.

Type 2 diabetes is characterized by obesity (particularly central deposition adiposity, or fat around the middle and deep in the abdominal cavity), cardiovascular disease, systemic inflammation, and the poor ability of muscles to store nutrients, which leads to muscle wasting and fat storage as well as nutrients circulating in the blood.

Insulin resistance, and its associated metabolic syndrome, is a step along the road to type 2 diabetes.

Like parents who may eventually tune out their screaming toddler, cells “tune out” insulin if insulin is chronically high. Since glucose is then poorly stored, people end up with both high circulating blood insulin and high circulating glucose.

Usually, they also end up with things like high triglycerides, high levels of “bad” LDL cholesterol, lower levels of “good” HDL cholesterol, higher levels of inflammatory proteins, and high blood pressure. Their blood is full of crud, their muscles aren’t getting properly nourished, and their body’s inflamed. It’s the perfect metabolic storm.

What you should know about insulin

Due to the anabolic power of insulin, many over-fat individuals want to avoid insulin release. This is because they want to avoid storing body fat. Well, as we already learned, you cannot avoid insulin in the blood.

You need insulin, but the trick is to learn how to balance the anabolic effects in muscle tissue against the fat storage effects. This can be done by increasing insulin sensitivity in the muscle while decreasing insulin sensitivity in the fat cells. Controlling insulin release during the day is important for long-term sensitivity.

What keeps insulin sensitivity high?

• Exercising 5 hours per week, especially resistance training
• Lots of muscle mass
• Higher intakes of vegetables, whole-grain foods, legumes, lean proteins, and nuts/seeds
• Supplements like omega-3 fatty acids, alpha-lipoic acid, and chromium
• Adequate vitamin D status
• Limiting caffeine intake
• Commuting to work via biking and/or walking
• Regular tea consumption
• 7-9 hours of sleep per night

What lowers insulin sensitivity?

• Low-carbohydrate, high-fat diets
• High processed carbohydrate diets
• Sedentary lifestyle
• Nicotine use
• Regular caffeine consumption
• Vitamin D deficiency
• Sporadic sleep patterns
• Excessive alcohol consumption

Summary and recommendations

• Participate in some form of resistance training and/or intense conditioning 4-5 times per week.
• Aim for a moderate carbohydrate consumption (~40% of diet) with an emphasis on fibrous carbohydrates like vegetables, fruits, legumes, and whole grains.
• Control fat intake (~20-25% of diet). Emphasize sources like nuts, seeds, olives, avocados, olive oil, flax oil, and fish oils.
• Investigate chromium and alpha lipoic acid, and make sure intake is adequate (but not excessive).
• Supplement with omega-3 fatty acids from algae or fish.
• Drink water or tea, and limit calorically dense beverages and alcohol.
• Make sure to get in the sun at least 20 minutes per day or use a vitamin D supplement.
• Make sure to get 7-9 hours of sleep per night.

For extra credit

Glycemic index and insulin index

While the glycemic and insulin indices of many foods are similar, some foods cause unexpected responses. Milk products have a lower glycemic index, but a very high insulin index. Rice has a higher glycemic index, but a lower insulin index. Keep in mind that a low glycemic diet can result in better fasted insulin and glucose, but results have been mixed.

Nutrient timing

The purpose of nutrient timing is to maximize insulin’s anabolic effects while minimizing its other problematic side effects.

Chromium

Chromium increases the presence of glucose transporters on the cell membrane. In theory, it may help manage blood sugar, but trials using chromium have shown mixed results.

Breast-feeding

Some epidemiologic studies have found that breast-feeding is associated with a reduced risk for developing insulin-dependent diabetes.

Early introduction of gluten-containing foods

Supplementing infant diets with gluten-containing foods before 3 months of age may encourage pancreatic dysfunction.

Nutrition and exercise patterns

Asian and African populations who are physically active and follow diets low in fat and high in fibrous carbohydrates have lower incidence of diabetes than those living the “Western” lifestyle.

Early introduction of cow’s milk

The American Academy of Pediatrics stated that avoiding early exposure to cow’s milk may reduce the risk of developing antibodies to cow’s milk protein and type 1 diabetes.

Alpha lipoic acid

Alpha lipoic acid may increase glucose uptake in the cell by recruiting glucose transporters.

Fat deposition patterns

Upper-body and central adiposity (in other words, fat around the middle and/or deep in the abdominal cavity) is strongly correlated with elevated insulin and, in excess, with metabolic syndrome.

Some people who are not obese by traditional measures are still at risk for insulin resistance anyway, particularly individuals with one or more close relatives who are diabetic, as well as many people of South Asian ethnic origin.

Insulin supplementation

Many bodybuilders have experimented with injecting insulin in an attempt to maximize insulin’s anabolic effects. This has sent more than one “home pharmacist” to the hospital, as even a little too much insulin in an injection can easily cause coma and death.

Further resources

The Anabolic Power Of Insulin

References

Moisey LL, et al. Caffeinated coffee consumption impairs blood glucose homeostasis in response to high and low glycemic index meals in healthy men. Am J Clin Nutr 2008;87:1254:1261.

Gordon-Larsen P, et al. Active commuting and cardiovascular disease risk: The CARDIA Study. Arch Intern Med 2009;169:1216-1223.

Guyton AC, Hall JE (2000) Insulin, glucagon, and diabetes mellitus. In: Textbook of Medical Physiology. Philadelphia: W. B. Saunders, pp. 884-898.

Craig WJ & Mangels R. Position of the American Dietetic Association: Vegetarian Diets. J Am Diet Assoc 2009:109:1266-1282.

Klimcakova E, et al. Dynamic strength training improves insulin sensitivity without altering plasma levels and gene expression of adipokines in subcutaneous adipose tissue in obese men. J Clin Endo Metab 2006;91:5107-5112.

Albright A, et al. American College of Sports Medicine position stand. Exercise and type 2 diabetes. Med Sci Sports Exerc 2000;32:1345-1360.

Chipkin SR, et al. Exercise and diabetes. Cardiol Clin 2001;19:489-505.

Colberg SR & Grieco CR. Exercise in the treatment and prevention of diabetes. Curr Sports Med Rep 2009;8:169-175.

Vitoria JC, et al. Association of insulin-dependent diabetes mellitus and celiac disease: a study based on serologic markers. J Pediatr Gastroenterol Nutr 1998;27:47-52.

Pastore MR, et al. Six months of gluten-free diet do not influence autoantibody titers, but improve insulin secretion in subjects at high risk for type 1 diabetes. J Clin Endocrinol Metab 2003;88:162-165.

Ziegler AG, et al. Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies. JAMA 2003;290:1721-1728.

Norris JM, et al. Timing of initial cereal exposure in infancy and risk of islet autoimmunity. JAMA 2003;290:1713-1720.

Wasmuth HE & Kolb H. Cow’s milk and immune-mediated diabetes. Proc Nutr Soc 2000;59:573-579.

Vaarala O. Is type 1 diabetes a disease of the gut immune system triggered by cow’s milk insulin? Adv Exp Med Biol 2005;569:151-156.

Virtanen SM, Knip M. Nutritional risk predictors of beta cell autoimmunity and type 1 diabetes at a young age. Am J Clin Nutr. 2003;78:1053-1067.

Ylonen K, et al. Dietary intakes and plasma concentrations of carotenoids and tocopherols in relation to glucose metabolism in subjects at high risk of type 2 diabetes: the Botnia Dietary Study. Am J Clin Nutr 2003;77:1434-1441.

Ford ES, Mokdad AH. Fruit and vegetable consumption and diabetes mellitus incidence among U.S. adults. Prev Med 2001;32:33-39.

Lopez-Ridaura R, et al. Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care 2004;27:134-140.

Montonen J, et al. Dietary antioxidant intake and risk of type 2 diabetes. Diabetes Care 2004;27:362-366.

Montonen J, et al. Dietary patterns and the incidence of type 2 diabetes. Am J Epidemiol 2005;161:219-227.

Liese AD, et al. Dietary patterns, insulin sensitivity, and adiposity in the multi-ethnic Insulin Resistance Atherosclerosis Study population. Br J Nutr 2004;92:973-984.

Cheng HH, et al. Antioxidant effects of chromium supplementation with type 2 diabetes mellitus and euglycemic subjects. J Agric Food Chem 2004;52:1385-1389.

Cefalu WT, Hu FB. Role of chromium in human health and in diabetes.
Diabetes Care 2004;27:2741-2751.

Kleefstra N, et al. Chromium treatment has no effect in patients with poorly controlled, insulin-treated type 2 diabetes in an obese Western population: a randomized, double-blind, placebo-controlled trial. Diabetes Care 2006;29:521-525.

Henriksen EJ. Exercise training and the antioxidant alpha-lipoic acid in the treatment of insulin resistance and type 2 diabetes. Free Radic Biol Med 2006;40:3-12.

Aston LM, et al. No effect of a diet with a reduced glycaemic index on satiety, energy intake and body weight in overweight and obese women. Int J Obes (Lond) 2008;32:160-165.

Haag M, Dippenaar NG. Dietary fats, fatty acids and insulin resistance: short review of a multifaceted connection. Med Sci Monit 2005;11:359-367.

Barnard ND, et al. A low-fat, vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes. Diab Care 2006;29:1777-1783.

Stroud ML, et al. Vitamin D – a review. Aust Fam Physician 2008;37:1002-1005.

Tai K, et al. Vitamin D, glucose, insulin, and insulin sensitivity. Nutrition 2008;24:279-285.

Boschmann M & Thielecke F. The effects of epigallocateghin-3-gallate on thermogenesis and fat oxidation in obese men: a pilot study. J Am Coll Nutr 2007;26:389S-395S.

Eichenberger P, et al. Effects of 3-week consumption of green tea extracts on whole-body metabolism during cycling exercise in endurance-trained men. Int J Vitam Nutr Res 2009;79:24-33.

Venables MC, et al. Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. Am J Clin Nutr 2008;87:778-784.

Grundy et al. Diagnosis and Management of the Metabolic Syndrome. Circulation. 2005;112:2735-2752. Published online before print September 12, 2005, doi: 10.1161/CIRCULATIONAHA.105.169404

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Why is vitamin D so important?

Nearly every tissue and cell in our body has a vitamin D receptor. Without enough activated vitamin D in the body, dietary calcium cannot be absorbed. Calcium is essential for signaling between brain cells, development of bone, and tooth formation. Let’s be honest, nobody likes rickets.

Studies also reveal that low vitamin D levels in the body are associated with:

• Increased loss of muscle strength and mass as we age
• Increased risk of cancers
• Lower levels of immunity
• Higher blood pressure
• The development of neurological disorders
• The development of diabetes

Alright, so we just spend more time in the sun or pop some supplements. Not so fast.

Despite the importance of vitamin D, it’s estimated that anywhere from 30% to 80% of the U.S. population is vitamin D deficient. It’s likely worse among people with darker skin living in northern zones, as their skin pigmentation screens out the relatively limited sunlight more effectively.

If your skin is darker, you are at higher risk of vitamin D deficiency. Consider spending more time at the beach. Get your doctor to write you a note -- hey, that surfing trip is for medical reasons!

Vitamin D levels can also be affected by age and body fat levels. As we age, our ability to make vitamin D is reduced by 75%. Furthermore, vitamin D can get trapped in body fat, leading to a 55% reduction in blood levels for those who are over-fat.

What you should know about vitamin D

Vitamin D is a fat soluble vitamin that exists in various forms. The animal form is vitamin D3 (cholecalciferol) and the plant form is vitamin D2 (ergocalciferol). Vitamin D2 and D3 are not biologically active; they must be modified in the body to have any effect.

The active form of vitamin D is indeed a hormone and is known as 1,25-dihydroxyvitamin D3 [1,25(OH)₂D3] or calcitriol. (Feel free to use that as a conversation starter the next time you’re picking up a hot date.) Both vitamin D2 and D3 have been commercially synthesized and both forms seem to be effective at maintaining blood levels of vitamin D in the body.

The sun

Vitamin D isn’t really a “true” vitamin, as we don’t need food to attain it. Natural sunlight allows our body to create vitamin D and even destroys excessive amounts. How does that happen?

Step #1: We convert cholesterol to 7-dehydrocholesterol, which is a precursor of vitamin D3.

Step #2: When we are exposed to UVB radiation, 7-dehydrocholesterol in the skin is converted to vitamin D3.

Step #3: Vitamin D3 must then be hydroxylated in the liver and the kidneys to become active. At this point, it can exert its endocrine effect.

Vitamin D metabolism

Think you’re soaking up vitamin D through office/car windows? Wrong. Glass blocks virtually all UVB, preventing vitamin D from being made.

And sunscreen is similar. Applying sunscreen with an SPF of 15 will decrease the amount of vitamin D made in the body by about 99%. Hooray for basal cell carcinoma prevention. But bummer for vitamin D production.

Activated vitamin D has a serum half life of 2-3 weeks and its production in the skin is limited to 10,000-20,000 IU each day. Spending 20 minutes riding your bike outside in the summer sun produces 100 times more vitamin D than government agencies say you need. And once serum levels reach 150 nmol/L, any excess is inactivated. Thanks be to Mother Nature.

Vitamin D production via the sun can change throughout the year depending on where you live. If you live north of Atlanta, GA, you will make zero vitamin D from the sunlight between November and March. If you live below Atlanta, GA, you’ll be all right. It is possible to build some reserves of vitamin D, but these reserves won’t last longer than a few weeks.

Get yourself one of these bad boys — a portable Vitamin D meter!

Food

Vitamin D is extremely rare in foods. It’s found in fish, cod liver oil, mushrooms, liver and eggs – but usually not in substantial amounts (except in cod liver oil).

Farmed varieties of fish contain very little vitamin D compared to the wild varieties. The only reason we even get vitamin D from foods like milk and cereal is because these foods are fortified with it — it doesn’t naturally occur.

Breast milk contains low amounts, with about 25 IU per liter.

Thus, getting enough vitamin D from whole foods is virtually impossible; it truly is the sunlight vitamin.

Fortification studies in adults show that consuming 100 – 1000 IU of vitamin D each day results in increased blood concentrations by 15 to 40 nmol/L. Other data with supplements indicate that for every 100 IU of vitamin D we ingest, we raise our blood levels by 2.5 nmol/L.

What should my blood levels be?

Now, while vitamin D is fun to talk about, what really matters is our circulating 25-hydroxyvitamin D [25(OH)D] concentration. It lets us know how much vitamin D has been produced in our body from sun, food and supplements. Its half-life is 15 days. 1,25 (OH)₂D is not a good indicator of vitamin D status, as it has a short half life of only 15 hours and levels in the blood are regulated tightly by hormones and minerals. 1,25 (OH)₂D only starts to decline when a severe deficiency of vitamin D is present.

The most advantageous serum concentrations of 25(OH)D seem to begin at 75 nmol/L, with the optimal levels being between 90 and 100 nmol/L. Most people will be unable to reach these levels with an intake between 200 and 600 IU of vitamin D.

What intake is optimal?

An intake of greater than or equal to about 1000 IU may be needed for most of the population. For postmenopausal women and older men, 25(OH)D concentrations of less than 30 to 80 nmol/L are associated with negative health outcomes.

For infants at northern latitudes, studies suggest that 200 IU vitamin D2 per day may not be enough to prevent vitamin D deficiency. A meta-analysis in adults suggested that an increased intake of vitamin D₃ of 100 IU per day was associated with an increase in circulating concentration of 25(OH)D of 1 to 2 nmol/L. A recent study on women in Maine found that 800 IU of vitamin D per day was enough to reach and maintain adequate blood levels during the winter (for most of the women).

Levels of 25(OH)D producing health benefit

What levels of vitamin D intakes are associated with adverse effects?

Most studies do not report adverse effects with vitamin D supplementation. One study showed an increased risk of kidney stones with supplemental intakes of 400 IU vitamin D3 (along with 1000 mg calcium) each day in women aged 50 to 79 years.

The Merck Manual notes:

Taking very high daily doses of vitamin D—for example, 50 or more times the recommended daily allowance (RDA)—over several months can cause toxicity and a high calcium level in the blood (hypercalcemia).

Early symptoms are loss of appetite, nausea, and vomiting, followed by excessive thirst, weakness, nervousness, and high blood pressure. Because the calcium level is high, calcium may be deposited throughout the body, particularly in the kidneys, blood vessels, lungs, and heart. The kidneys may be permanently damaged and malfunction, resulting in kidney failure.

Some studies suggest that intakes up to 10,000 IU per day have not been associated with adverse effects. If you take more than 10,000 IU per day of vitamin D orally for more than 6 months, you are definitely at risk of becoming vitamin D intoxicated. And remember, we cannot become vitamin D intoxicated from excessive sunlight.

Summary and recommendations

Vitamin D deficiency is a disease of neglect. It’s up to us to get in the sun and/or use a supplement as needed. And the data seem to be pointing towards reaching “optimal” levels, not just “normal” levels.

Blood level classifications for 25(OH)D:

• Vitamin D intoxication: >/= 375 nmol/L
• Preferred range: 75-100 nmol/L
• Insufficient range: 50-75 nmol/L
• Mild deficiency: 25-50 nmol/L
• Moderate deficiency: 12.5-25 nmol/L
• Severe deficiency: <12.5 nmol/L

The total requirement for vitamin D (sun and food) is about 4000 IU/day to keep 25(OH)D levels above and/or around 100 nmol/L. Treating deficiency can require more. To normalize stores, adults require 3000-5000 IU per day for 6 to 12 weeks. As the potential for toxicity is present, work with your physician when beginning a supplementation regimen.

Full recommendations can be found in PN Version 3.0. They are very specific, so read them carefully. We will reprint them below:

Vitamin D (D2 is plant, D3 is animal)
South of LA/Dallas/Atlanta/Cairo

• 15-30 minutes of mid-day sun (15 for those with lighter skin, 30 for darker skin)
• OR 4,000 IU supplemental vitamin D2 daily

Around Portland/Chicago/Boston/Rome/Beijing

• From February – November
• 15-30 minutes of mid-day sun (15 for those with lighter skin, 30 for darker)
• OR 4,000 IU supplemental vitamin D2 daily
• From December – January
• 4,000 IU supplemental vitamin D2 daily

Around Edmonton/London/Berlin/Moscow

• From March – October
• 15-30 minutes of mid-day sun (15 for those with lighter skin, 30 for darker)
• OR 4,000 IU supplemental vitamin D2 daily
• From November – February
• 4,000 IU supplemental vitamin D2 daily

North of Edmonton/London/Berlin/Moscow

• From April – September
• 15-30 minutes of mid-day sun (15 for those with lighter skin, 30 for darker)
• OR 4,000 IU supplemental vitamin D2 daily
• From November – February
• 4,000 IU supplemental vitamin D2 daily

When using vitamin D supplements also consider adiposity, physical activity, baseline vitamin D and calcium status, oral contraceptive use, and race-ethnicity. All of those factors can impact needs.

For extra credit

During the winter, very little UVB reaches us, and thus, less cholesterol is used to synthesize vitamin D in the body. This is one of the reasons blood cholesterol levels may be higher during the winter months.

Serum 25(OH)D is the best indicator of vitamin D status.

Using a multi-vitamin to get vitamin D can be a problem. By the time enough vitamin D is consumed, you will reach toxic levels for other vitamins/minerals.

25(OH)D was isolated in 1970.

Why are vitamin reviews triggered in the IOM-sponsored DRI Committees? Funding. Remember that we need to maintain a separation between funding decisions and the essential autonomy of scientific process.

Some data has indicated a link between Crohn’s disease and vitamin D deficiency.

Vitamin D may help with alleviating psoriasis.

Some research has demonstrated that vitamin D supplementation may be immunosuppressive.

A classic sign of vitamin D deficiency is isolated and generalized muscle and bone pain.

Medications can decrease activity of vitamin D in the body. These include anticonvulsants, bile acid sequestrants, GERD medications, corticosteroids and heparin. There is also some potential negative interactions with calcium channel blockers and diuretics, which can interfere with blood calcium levels.

People with dark skin may require 5-10 times the amount of sun exposure to produce adequate vitamin D, compared to someone with light skin pigmentation.

A recent study suggested that vitamin D can help prevent cancer. The researchers write: “Raising the minimum year-around serum 25(OH)D level to 40 to 60 ng/mL (100–150 nmol/L) would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three fourths of deaths from these diseases in the United States and Canada… Such intakes also are expected to reduce case-fatality rates of patients who have breast, colorectal, or prostate cancer by half. There are no unreasonable risks from intake of 2000 IU per day of vitamin D3 , or from a population serum 25(OH)D level of 40 to 60 ng/mL.”

Further resources

Vitamin D Lecture

Vitamin D Council

References

Yetley EA, et al. Dietary Reference Intakes for vitamin D: justification for a review of the 1997 values. Am J Cline Nutr 2009;89:719-727.

Bischoff-Ferrari HA, et al. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 2006;84:18-28.

Moalem S. Survival of the Sickest. 2007. William Morrow Publishers.

Ginde AA, et al. Association between serum 25-hydroxyvitamin D level and upper respiratory tract infection in the third national health and nutrition examination survey. Arch Intern Med 2009;169:384-390.

Aloia JF, et al. Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Am J Clin Nutr 2008;87:1952-1958.

Stroud ML, et al. Vitamin D: A Review. Aust Fam Phys 2008;37:1002-1005.

Michael Holick Vitamin D Pioneer Interview. Alternative Therapies 2008;14:64-75.

Vieth R, et al. The urgent need to recommend an intake of vitamin D that is effective. Am J Clin Nutr 2007;649-650.

Schwalfenberg G. Not enough vitamin D: Health consequences for Canadians. Canadian Family Physician 2007;53:841-854.

Vieth R & Fraser D. Vitamin D insufficiency: no recommended dietary allowance exists for this nutrient. CMAJ 2002;166:1541-1542.

Higdon J. An Evidence Based Approach to Vitamins and Minerals. The Linus Pauling Institute. 2003. Thieme, New York.

Ward KA, et al. Vitamin D status and muscle function in post-menarchal adolescent girls. J Clin Endocrinol Metab 2009;94:559-563.

Heaney RP, et al. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr 2003;77:204-210.

Dietary Supplement Fact Sheet: Vitamin D. NIH Office of Dietary Supplements. Accessed 3/10/09.

Mora JR, et al. Vitamin effects on the immune system: vitamins A and D take centre stage. Nature Reviews Immunology 2008;8:685-698.

National Academy of Sciences. Beyond Discovery. Unraveling the Enigma of Vitamin D. Accessed 3/11/09.

Penckofer S, et al. Vitamin D and diabetes. Let the sunshine in. The Diabetes Educator 2008;34:939-954.

Nelson ML, et al. Supplements of 20 mcg/d cholecalciferol optimized serum 25-hydroxyvitamin D concentrations in 80% of premenopausal women in winter. J Nutr 2009;139:540-546.

Garland CF, Gorham ED, Mohr SB, Garland FC. Vitamin D for cancer prevention: global perspective. Ann Epidemiol. 2009 Jul;19(7):468-83.

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Estrogen is often thought of as the “female sex hormone”, but in fact it’s prevalent in both men and women.

There are actually a few forms of estrogen — the term usually refers to a family of steroid hormones that are synthesized in a variety of tissues.

• Estradiol (sometimes known as E2) is the most potent estrogen. In women it’s produced by the ovaries.
• Estriol (sometimes known as E3) is produced during pregnancy. Non-pregnant women don’t make much of it at all.
• Estrone (sometimes known as E1) is the most dominant estrogen in menopausal women.

Most often when people talk about “estrogen” they really mean estradiol. Estrone and estriol have about one tenth the potency of estradiol.

How our bodies make estrogens

Estrogens, like other sex hormones, are derived from cholesterol. They’re created by the aromatization (conversion) of androgens in an intricate process.

It’s easy to assume that so-called “male hormones” and “female hormones” are “opposites”. In fact, as the diagram below shows, the early stages of synthesizing estradiol and testosterone (and other androgens) are exactly the same!

Estradiol is formed if the substrate is testosterone, whereas estrone results from the aromatization of androstenedione.

In pre-menopausal women, the most important producer of estrogens are the ovaries. In post-menopausal women (whose ovaries have gradually ceased production), adipose (aka fat) tissue also plays a role. In men, the main source of estrogen is testosterone that has aromatized.

Because fat tissue can produce hormones, excess body fat can disrupt proper hormonal balance.

Regulating estrogen

So what signals estrogen release? Well, the hypothalamus secretes a hormone known as gonadotropin-releasing hormone (GnRH). GnRH regulates luteinizing hormone (LH) and follicle stimulating hormone (FSH) release from the pituitary gland. LH and FSH stimulate secretion of estrogen from the ovaries.

Estrogen is released in pulses at intervals of 1 to 3 hours.

Hormones can circulate in the body in both “bound” and “unbound” forms. Bound hormones are attached to something else, e.g. a transport protein such as sex hormone binding globulin (SHBG). (Imagine a bunch of kids hitching a ride on an inner tube as it’s pulled down a lazy river ride and you’ll get the idea.) Unbound hormones circulate freely.

Once released, only unbound estrogen appears to be biologically active.

Why are estrogens so important?

Estrogens are essential regulators of many major processes in the body. For example:

• They strongly influence the deposit of body fat — both amount and location.
• They also influence muscle mass.
• Estradiol has cardioprotective properties via changes in vasculature and other tissues. This is why premenopausal women have much lower rates of cardiovascular diseases than men — but their risk sharply increases after menopause.
• Estrogen acts on bone to determine the overall balance of breakdown and formation. Estrogen inhibits bone breakdown and may stimulate bone formation by initiating synthesis of IGF-1. After estradiol withdrawal during menopause (and with exercise induced amenorrhea in young female athletes) the pace of bone breakdown becomes limited, and mechanical loading is effective only in bones that are exposed to stress.

The menstrual cycle

Estradiol levels (red line in diagram below) normally fluctuate during a woman’s menstrual cycle, peaking just before ovulation and falling around the time of menstruation.

Researchers have explored whether these cyclical changes have effects on exercise performance, wellbeing, and body composition.

Stress hormones

The menstrual cycle has little effect on the secretion of stress hormones such as growth hormone during exercise. When exercise takes place at times when estradiol levels are higher, cortisol secretion is either unaffected or suppressed. Aldosterone secretion is higher at these times and may contribute to increased fluid retention.

Fuel use

Estrogen variations during the menstrual cycle have a minimal effect on fuel utilization. Lipid utilization may be higher during the luteal phase following ovulation.

High estradiol is associated with decreased fat storage enzyme activity. High estradiol also contributes to higher HDL levels (aka the “good cholesterol”, which is cardioprotective).

Estradiol increases free fatty acid and triglyceride content of muscle and fat tissue, inhibits fat storing enzymes, and increases fat mobilizing enzymes during exercise.

Thermoregulation

Core temperature is lowest during ovulation and highest during the luteal phase of the cycle. During the luteal phase of the menstrual cycle, thresholds for vessel dilation and sweating increase.

Appetite, hunger and satiety hormones

CCK (cholescystokinin) mediates estradiol-induced suppression of appetite during menstrual cycles.

Male and female reproductive hormones exert a differential effect on leptin expression, which results in greater circulating leptin levels in women (higher leptin is associated with appetite suppression).

Body fat

An increase of the masculinizing hormones along with a decrease of estrogen in women is associated with higher levels of intra-abdominal body fat (often known as the “apple shape”). You may also know that insulin resistance is associated with accumulation of intra-abdominal body fat.

What you should know

Normal serum levels:

Men, women, and estrogens

Considerable amounts of estrogens are formed by the aromatization of androgens.

In males, the aromatization of testosterone to estradiol accounts for 80% of what is produced. In females, nearly 50% of the estradiol created during pregnancy comes from the aromatization of androgens. The conversion of androstendione to estrone is the foremost source of estrogens in post-menopausal women.

Aromatase is an enzyme that’s required to convert androgens to estrogens. It’s active in adipose cells, liver cells, skin cells, and other tissues. With excess body fat, production of estrogen (and other hormones and cell signalers) increases. This is why many health conditions such as gynecomastia (male breast growth), reproductive disorders, and breast cancer are linked to obesity — as well as why aromatase inhibitors are often prescribed for these conditions.

The role of fat in estrogen production

Exercise of moderate to high intensity is associated with increases of sex hormones in a gender specific fashion. Males display little change of estradiol and estrone in response to exercise.

In women, increases of estrogen are proportional to exercise intensity and more prominent during the luteal phase than during the follicular phase of the menstrual cycle. Increases in plasma progesterone occur during the luteal phase of the cycle only.

For extra credit

Estradiol levels decline rapidly during the first week after birth and remain at about 8 to 10 pg/mL in females and males until onset of puberty.

Estrogens are bound to SHBG. SHBG binds estradiol about five times less avidly than it binds testosterone.

Changes in estrogen levels with age

During pregnancy, at moderate intensity exercise, estradiol secretion is increased, more so in the later stages of pregnancy.

17% fat is the threshold of body fat necessary for the onset of menarche, and 22% fat is the threshold level of body fat necessary for the maintenance of fertile menstrual cycles. This relationship proposes that female fertility is dependent on the availability of 99,000 calories contained in 11 kg of body fat, enough to provide the 80,000 calories needed for a full-term pregnancy.

Acute reduction in energy availability to less than 25 kcal/kg of lean body mass (via exercise), precipitates reductions in LH pulses. Reduction of LH pulsatility is more severe after dietary restriction than after increased energy expenditure from exercise. Changes in LH pulsatility in exercising women are prevented when increased food intake adequately compensates for the energy cost of exercise. · At least four different mechanisms may contribute to development of exercise-induced amenorrhea.

• Effects of acute energy drain
• Level of body fat stores
• Increased levels of inappropriate sex steroids
• Increased levels of stress hormones

At submaximal exercise intensities, women release and oxidize more fat tissue and rely less on muscle lipids and glycogen than do men.

Males need estrogen during fetal development — it actually masculinizes the brain.

There are also other forms of estrogen-like compounds, such as those found in plants like soy (aka phytoestrogens), or xenoestrogens with estrogen-like actions that occur in things like plastics or pesticides. There are even mycoestrogens, made by fungi!

Summary and recommendations

To maintain healthy estrogen levels:

• Eat enough quality calories
• Avoid bouts of overtraining
• Be aware of exercise intensity throughout pregnancy
• Maintain a healthy body fat level
• Avoid use of exogenous androgens
• No fad dieting

References

Beers MH, Berkow R eds. Merck Manual. 17th ed. Merck Research Laboratories. Whitehouse Station, NJ. 1999.

Murray RK, Granner DK, Mayes PA, Rodwell VW, eds. Harper’s Illustrated Biochemistry. 26th ed. McGraw Hill. 2003.

Borer KT. Exercise Endocrinology. Human Kinetics. Champaign, IL. 2003.

Harvey RA, Champe PC eds. Pharmacology 2nd ed. Lippincott Williams & Wilkins. 2000.

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