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Doctor Detective with Bryan Walsh


In this week’s case, Dr. Detective investigates why a healthy client is dealing with the symptoms of reactive hypoglycemia, and provides a simple prescription for maintaining stable blood sugar levels and cognitive function.

Eat less and exercise more. It’s generally a great prescription for improving health and improving body composition. However, it doesn’t always work.

Even with an awesome exercise plan and a rock-solid diet, some people suffer from mysterious symptoms and complaints that seem puzzling.

When we meet clients who have problems that exercise and nutrition – not to mention their own doctors – can’t seem to solve, we know there are only a few experts on the planet to turn to. One of them is Bryan Walsh.

Dr. Walsh has a sharp mind, a fitness background, a degree in naturopathic medicine, and extensive additional training and certifications. His wife is a naturopath too. (We bet his kids are the healthiest on the planet.)

When tough cases arise, Dr. Walsh turns from mild-mannered dad and husband into forensic physiologist. He pulls out his microscope, analyzes blood, saliva, urine, lifestyle – whatever he has to, in order to solve the medical mystery.

When Dr. Walsh volunteered to work on a regular case study feature with us, we jumped at the chance. By following along with these fascinating cases, you’ll see exactly how a talented practitioner thinks. You’ll also learn how to improve your own health.

In today’s case, you’ll meet a young mother whose low blood sugar made her irritable, mentally foggy, and frustrated, but who was helped by a prescription of water, sea salt, digestive enzymes, fatty acids – and L-carnitine.  Find out how Dr. Detective cracks the case.

Hyper- vs hypoglycemia

Insulin resistance. Metabolic syndrome. Diabetes. Serious — and increasingly common — disorders of blood sugar regulation that many people in the general population know and fear.

These problems are often characterized by hyperglycemia — too much blood sugar (glucose) circulating at once.

Yet another whole subset of the population struggles with hypoglycemia — periods of not enough blood sugar.

For a Type 1 insulin-dependent diabetic, hypoglycemia caused by an insulin overdose can be life-threatening.

For a normal, relatively healthy person, hypoglycemia is usually just an annoying inconvenience. Although one that’s easily remedied if you understand basic physiology.

The mechanics of blood sugar regulation

Insulin, released from the pancreas in response to a meal, is the primary hormone responsible for lowering blood sugar levels.

But there are as many as four hormones involved in raising blood sugar levels:

  • glucagon;
  • cortisol;
  • growth hormone (GH); and
  • adrenaline (aka epinephrine, norepinephrine)

Our bodies use adrenaline when the other three don’t work.


When the brain’s “glucostat”, or blood sugar level sensor, decides that blood sugar is too low and the other hormones aren’t doing their jobs properly, it’ll tell the adrenal glands to release the emergency brakes.

Adrenaline kicks in for a quick release of blood sugar. You get the jitters, shakes, irritability, “brain fog”, a sense of “oh my gawd I have to eat now” panic, and sometimes (if the problem happens overnight) the early-morning “blast out of bed” wakeup.

You would think, with four hormones available to do the lifting, blood sugar levels would rarely dip too low. Yet for some people, mysteriously, that doesn’t seem to be the case. Their bodies seem to panic and grab that adrenaline emergency lever a little too readily.

Some people suffer from reactive or post-prandial hypoglycemia — a sudden drop in blood sugar within an hour or two after a meal.

Keeping things balanced

Fortunately, these types of mild hypoglycemia are relatively easy to correct with some simple steps:

  • Eat small meals at regular intervals — every 2-4 hours is usually about right.
  • If you include carbohydrates in a given meal, choose higher-fiber, slow-digesting carbohydrates (such as vegetables, beans/legumes, etc.).
  • Balance protein, fat, and slow-digesting carbohydrates (since many people find that a mostly-protein or mostly-carbohydrate meal can touch off hypoglycemic episodes).

But why does the problem happen in the first place?

This week’s case gave me an opportunity to work out a hypothesis.

The client

31-year-old Kate was an active, athletic, mother of three young children who’d been health-conscious and fit since adolescence. That made her symptoms all the more confusing.

When she first visited us at the clinic, Kate was still nursing her third child. I made a note of that, since this would limit the kinds of supplements we might feel comfortable recommending.

The client’s signs and symptoms

In general, Kate felt relatively healthy. Yet she suffered from:

  • digestive difficulties, especially when eating fatty meals;
  • shakiness and irritability between meals; and
  • brain fog, forgetfulness, and a sense that she wasn’t mentally “on her game”.

What could be going on?

Overall, Kate was a healthy eater. But she admitted that with three young kids at home, she sometimes took her snacks when she could get them, rather than according to a schedule.

She also mentioned frequent thirst.  She’d pour herself a glass of water, but then, in the bustle of her day, forget to drink it.

Kate exercised at the gym 4-5 times a week and got adequate sleep, but she often felt tired, as if she could have slept a lot longer.

The tests and assessments

Lots of young mothers feel tired. Lots of young mothers miss the occasional meal. And far too many of them, these days, suffer from symptoms like Kate’s.


Like any good detective, once I had the patient’s history, I sent her for some blood work.

The test results

Blood chemistry panel

Kate’s blood chemistry panel revealed some important clues:

Marker Result Nutritional reference range Thoughts
BUN 11 mg/dL 13.0-18.0 Low-normal – possibly poor protein digestion/absoprtion
RBC 4.53 x10^12/L 3.9-4.5 High-normal – usually dehydration and/or elevated testosterone
Hemoglobin 14.9 g/dL High-normal – usually dehydration and/or elevated testosterone
Hematocrit 44.7% High-normal – usually dehydration and/or elevated testosterone
MCV 99 fL Elevated – possible vitamin B12 and/or folic acid deficiency
Albumin 4.0 g/dL 4.0-5.0 Low-normal – possible inflammation; possibly poor protein digestion/absorption
LDH 129 IU/L 140-180 Low – possible tendencies towards reactive hypoglycemia
HDL cholesterol 79 mg/dL >50 High-normal – possible inflammation
Sodium 134 mmol/L 135-140 Low-normal – possible low adrenal (eg. aldosterone) output
Potassium 4.6 mmol/L 4.0-4.5 High-normal – possible low adrenal (eg. aldosterone) output

Based on Kate’s symptoms and blood work, I was beginning to put together a picture:

  1. Sub-optimal digestion:  This one was pretty obvious. The fact that Kate didn’t tolerate fats, together with a couple of the blood chemistry markers, made it pretty clear. (Note: in taking her history, I’d learned that for some years, Kate had followed a low-fat diet. This can increase one’s risk for gallstones and poor bile secretion for fat digestion – a factor I naturally had to consider.)
  2. Dehydration: Kate admitted to feeling thirsty and not drinking enough water.  That, combined with some of the blood chemistry markers (e.g. RBC, hemoglobin, hematocrit, sodium, potassium), and an in-office urinalysis (e.g. low specific gravity, indicating overly dilute urine), suggested that she was quite dehydrated.
  3. Reactive hypoglycemia: Kate’s low-normal LDH, along with the way she felt when she missed meals, pointed to a pretty strong tendency towards reactive hypoglycemia, or periods of low blood sugar.

Kate also showed a few more markers not described here, including slightly elevated eosinophils (a type of white blood cell) that might indicate an allergic reaction or a bacterial or parasitic infection. But even without further testing, I felt it was safe to get started on treatment.

The prescription

Again, Kate was nursing. So we needed to find the simplest, most elegant, safest solution to her problems. Just what a detective does best.


Not only did Kate need to drink more water, but we also asked her to add 1/8-1/4 tsp (1-2 g) of sea salt per liter of water.

Why sea salt? Based on her labs, it appeared she wasn’t retaining water due to possible low-normal aldosterone levels.  Sea salt, with its sodium and its valuable trace minerals, would help to address this.

Digestive enzymes

We asked Kate to take 2-3 capsules of Digestzyme (Designs for Health) with each meal.

Fatty acids

Due to what appeared to be poor fat digestion and absorption, we also prescribed a balanced fatty acid supplement (Optimal EFA by Biotics, 1 tsp per day).


We encouraged Kate to eat more regular meals including lean protein at each one, and gave her 2,000 mg of L-carnitine a day in divided doses. (We chose CarniClear by Designs for Health.)

Why L-carnitine? Here’s a short explanation. (Also see “Editor’s note” below.)

The carnitine-hypoglycemia story

Carnitine is a nitrogen-containing non-protein compound that can be synthesized by the body. Carnitine is thought to help transport long chain fatty acids across the inner mitochondrial membrane to be used as a source for ATP synthesis (beta oxidation).

Conventional nutritional wisdom suggests that because our body can make carnitine, we should easily have enough. But this assumes we have the necessary ingredients. To make carnitine, we need the amino acids lysine and methionine, as well as vitamin C, vitamin B6, iron, and oxygen. Many people lack one or more of these raw materials.

Carnitine can also be consumed in our diet, with the highest amounts occurring in red meat and pork. Some diets may be deficient.


When our blood sugar starts to drop between meals, two processes should kick in to help maintain normal levels – glycogenolysis and gluconeogenesis. The pancreatic hormone glucagon is thought to stimulate these processes.

But glucagon doesn’t seem to work correctly in hypoglycemics. What could be going on?

First, a quick review of the pathways:

  1. When glucose starts to drop, insulin will often drop and glucagon will often increase.
  2. This situation (low insulin, high glucagon) can stimulate lipolysis, or the liberation of fatty acids from adipocytes (fat cells).
  3. These fatty acids can make their way to the liver to be used for energy (ATP) synthesis.
  4. Fatty acids must enter into the mitochondria of cells, where they will be broken down into acetyl coenzyme A (acetyl-CoA), and used to produce ATP in the citric acid cycle.
  5. During low energy states, (e.g. low glucose), high levels of acetyl-CoA up-regulates the enzyme pyruvate into oxaloacetate, which can then be converted into phosphoenoylpyruvate (PEP) and used in hepatic gluconeogenesis. Conversely, low levels of acetyl-CoA down-regulates pyruvate carboxylase and thus gluconeogenesis will suffer.

So why, during low energy states, can acetyl CoA levels drop within the mitochondria?

Enter carnitine

During periods of low glucose, carnitine helps break down fatty acids into acetyl-CoA in the mitochondria and shuttles long chain fatty acids across the inner mitochondrial membrane.

Without carnitine, these changes  won’t occur and acetyl-CoA levels may drop. Thus low carnitine can lead to low levels of acetyl-CoA and effectively inhibit new glucose production.

(As a side note, glycogen phosphorylase, the enzyme necessary for converting stored glycogen into glucose, also requires vitamin B6, and thus may also play an unacknowledged role in hypoglycemia.)

Carnitine deficiency is relatively common during and after pregnancy, and in vegetarians. Given that Kate was a “health-conscious” eater as well as a fairly new mother of three, this might have played a role.

The outcome

Just a few days after starting our short protocol, Kate reported feeling much better.

Her digestion had improved and she felt less thirsty, but she was happiest about her improved cognitive function and the total absence of low blood sugar symptoms between meals.

In fact, she couldn’t believe how sharp she felt. She’d been feeling out of sorts for so long that she’d forgotten what it was like to be mentally alert and physically regulated.

Summary and recommendations

What can we take away from Kate’s story?

  1. Hydration is not just a matter of how much water we drink, but of how much water we retain. Specific hormones, as well as electrolyte balance, play a role in regulating this. Drinking lots of water isn’t always enough to ensure adequate hydration. And good hydration is key to maintaining other body functions, including glucose levels.
  2. Proper blood sugar regulation is paramount for proper functioning of virtually every system in the body, but stable blood sugar control is particularly important for optimal brain function.
  3. Despite the body’s many checks and balances, many people seem unable to maintain stable glucose.  Sometimes a sub-clinical carnitine deficiency contributes by preventing fatty acids from fueling the mitochondria and helping to clear gluconeogenesis pathways.
  4. If you’re a fitness-conscious “healthy eater”, good for you! High fives! However, do be aware that despite smart food choices, you may be missing some important nutrients, especially during times of greater need (such as pregnancy, injury recovery, other stress, etc.). May we suggest getting guidance from one of our coaching programs or working with one of our PN-certified professionals?


Editor’s note re: carnitine

Carnitine is found in nearly every cell of your body, and it plays a critical role in energy production. It’s most highly concentrated in heart and skeletal muscle and plays an important functional role in both tissues, transporting fatty acids into the mitochondria so these fats can be oxidized for energy.

Carnitine also transports toxic compounds generated during energy production out of the mitochondria to prevent them from accumulating. So carnitine not only produces energy, it cleans up after itself!  And this combination means that carnitine can be helpful after a cardiac event.

Carnitine controversy?

So what should we make of the recent study linking carnitine to heart disease? (And the subsequent media crusade suggesting that carnitine might cause heart disease.)

Well, to be honest, not much.

You see, to begin with, the researchers begin with the idea that red meat is associated with heart disease, basing their assumption on a couple of earlier studies. Since red meat is far and away the richest source of carnitine in the North American diet, this is a key part of their argument.

Yet one of the studies they rely on shows no such association!

That study, which compiled data from 20 epidemiological investigations dealing with red meat, cardiovascular disease, and diabetes, and involved over 1.2 million people, clearly stated that processed red meat had only a weak association with cardiovascular disease, and that:

Red meat intake was not associated with CHD (coronary heart disease)… or diabetes mellitus.”

So, the most massive analysis to date of the relationship of red meat to heart disease found absolutely no association — which essentially means that the recent carnitine study was founded on a flawed premise from the outset!


What’s more, the subject of the recent study was a chemical compound called TMAO (not to be confused with LMAO) which is raised by carnitine consumption.

The researchers suggest that since carnitine may increase TMAO, and that TMAO is associated with heart disease, carnintine might lead to an increased risk of heart disease.

Unfortunately for their argument, the data linking TMAO levels and cardiovascular disease are purely observational. In other words, we don’t actually know if there is any cause and effect relationship between the two.

No randomly controlled trial has ever shown that eating red meat contributes to cardiovascular disease, and randomly controlled trials are the only way we can draw reliable conclusions.

At this point, it’s all speculation.

Interestingly, when it comes to TMAO levels, carnitine-containing red meat is hardly the only food that raises them. Nor does it even come close to raising them the most!

Guess what causes the largest increase in TMAO levels: Fish!  That’s right: heart-healthy fish.

In fact, eating beef (as opposed to isolated carnitine) barely raises TMAO levels at all.  Bread, cauliflower, cabbage, mushrooms, and peas have all been observed to raise TMAO levels more than beef.

Do they cause heart disease too?

Bottom line? This study did little more than bring attention to some unproven associations. It did not show cause-and-effect.

Carnitine’s cardiac benefits

Indeed, there is already abundant data on the heart benefits of carnitine! Evidence like the following:

  • A concurrent study showing that… “L-carnitine significantly improves cardiac health in patients after a heart attack.”
  • Another study demonstrating that when chronic heart disease patients were given L-carnitine for a year, rates of death and chronic heart failure went down.
  • Studies showing that L-carnitine improves exercise capacity in patients with heart failure.

We hope this short analysis helps put to rest any concerns you might have about carnitine.

Carnitine can be a valuable supplement when used appropriately and in the right situations. (And if you already include the occasional grass-fed steak as part of your healthy PN-style routine, keep on enjoying it!)

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