There’s been a fair amount of hoo-hah in the nutritional web-o-sphere as of late regarding the “fattening” properties of dietary carbohydrates, what with the rise of the Paleo/Primal movement, French Dukan hype, LCHF (low carb high fat) and the old Atkins Diet Revolution movement reliving another moment of glory. The Scandinavians are certainly on board1, with Swedish and Danish bread producers feeling the toll3.
Don’t get me wrong, I think the reliance on starchy processed foods and an acceptance of saturated fats back into the diet is a superb idea, but such carb-phobia and panic that a whole macronutrient group is single-handedly fattening? Well that’s just absurd.

Now we’ve finally got it out of our systems that saturated fat and cholesterol aren’t to blame for modern disease, I feel like we’re sorely in danger of missing the point yet again, and demonizing another single nutrient as a scapegoat for the cataclysmically detrimental effects of the modern diet.

Question 1: Do carbohydrates raise insulin levels, and does insulin cause fat storage?

The carbohydrate-bashing is rooted in the belief that eating carbohydrates elevate levels of insulin, a hormone that has been suggested to promote fat storage. Gary Taubes, in his book Good Calories, Bad Calories, points the blame at carbohydrates (both refined and unrefined) as agents of obesity because of this very hypothesis:

“Carbohydrates, and particularly refined carbohydrates, are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity… Carbohydrates literally make us fat, and by driving us to accumulate fat, they make us hungrier and they make us sedentary” ~ Gary Taubes, Good Calories, Bad Calories

I think I’d almost quite like this to be the case. The carbohydrates = obesity idea is endearingly simple, but, just like the calories in = calories out theory, it doesn’t take into account the intricate web of cross-linked metabolic, nervous and hormonal responses within the human body that account for energy production, storage and expenditure.

To quickly explain the primary role of insulin in the body – it is to manage circulating concentrations of nutrients (principally glucose and fatty acids, the body’s two main fuels), keeping them within a fairly stable range, preventing us from entering either a hypoglycaemic (low blood glucose) state or a hyperglycaemic (high blood glucose) state. Insulin coordinates the metabolic shift from one type of fuel to the other, and back again. Any time insulin suppresses fat oxidation (use for energy), it increases carbohydrate oxidation by an equivalent amount. Insulin has a huge role to play, and a pretty useful one at that.

According to Taubes, the insulin spike that occurs after a high-carbohydrate meal causes fat storage and also causes stimulated food intake (ie, carbohydrates supposedly make us want to eat more). But studies have shown that satiety (feeling full and satisfied after a meal) actually increases with the degree of insulin release4 5, which is not consistent with Taubes’ theory. Also, it is worth noting that low-carbohydrate, high-protein meals can also have an insulin spiking effect, to an equal or sometimes even greater degree than high-carbohydrate meals6. The underlying message is this: both carbohydrates and proteins can spike insulin, and the insulin spike correlates positively with a feeling of satiety, reducing the desire to eat more and keeping us fuller for longer.

The claim that elevated insulin levels cause us to store fat and thereby become obese is not backed up by studies either, where increasing circulating insulin in animals reduces food intake and body weight in non-diabetic animals7 8 9 (possibly via an overlapping function with the satiety hormone leptin). Suppressing insulin receptors in the brain leads to increased fat mass in rodents10, suggesting that insulin’s normal function involves constraining fat mass. Insulin is also co-secreted with amylin, which suppresses food intake and body weight11. In fact, insulin is actually viewed by many obesity researchers as an anti-obesity hormone, not as an agent of obesity.

“The fact is, insulin spikes after meals temporarily decrease fat release from fat cells, but if you look at total 24 hour energy balance, insulin spikes, in conjunction with all the other hormones that are released in response to food ingestion, do not cause fat accumulation.  This is exactly how you would expect the system to work if it were designed to constructively handle a wide variety of macronutrient ratios, which it is.  Just as cholesterol did not evolve to give us heart attacks, insulin did not evolve to make us fat.” Dr Stephan Guyenet, Whole Health Source

All this aside, the bigger picture is the same as before, we can’t annihilate one single nutrient (or in this case, hormone) as the mechanism for human obesity. We can’t just suggest that body fatness solely revolves around insulin, and not consider amylin, glucagon, GLP-1, ghrelin, leptin, stomach distension, and all of the other short- and long-term signals that are activated in response to eating and also changes in body fat mass. These hormones and other factors all regulate food intake and body fatnesstogether, via the brain.

Question 2: were original hunter-gatherer diets low carbohydrate? And does this mean carbohydrate-restricted diets are optimal?

“Agricultural and pastoral humans have undergone significant genetic adaptations since the development of agriculture/pastoralism…  Evolution is a continuous process that has shaped our ancestors’ genomes for every generation since the beginning of life.  It didn’t end with the Paleolithic, in fact it accelerated, and most of us today carry meaningful adaptations to the Neolithic diet and lifestyle” ~ Stephan Guyenet

Most Asian countries, including China, Japan, Taiwan and India, have a traditional diet that is very high in carbohydrate (and in many cases, the dominant carbohydrate is white rice, a refined carbohydrate). Yet traditional Japanese, Chinese and Southern Indians eating mostly white rice were renowned for their leanness. To me, the idea that carbohydrates themselves cause insidious weight gain is just not plausible, given these observations.

If you go back further, to our hunter-gatherer Paleolithic roots, humans were already well adapted to eating carbohydrates. According to this study12, we show irrefutable genetic evidence for good carbohydrate tolerance. We’ve eaten high carbohydrate diets for thousands of years.

But apart from this evidence, I believe that it’s ultimately narrow-minded to look at specific hunter-gatherer-style diets as macronutrient ratio points of reference for how we should eat today, as they differ so wildly according to geography as to what was available for consumption. The fact is, to avoid extinction, humans are highly adaptable, with metabolisms well suited to be very tolerant of differing macronutrient ratios*. Our bodies will appropriately respond to differing carbohydrate-to-fat-to-protein ratios, and insulin is central to this response. Historic populations have thrived on both high-carbohydrate (eg Kitavans13 14) as well as high fat (eg Masai15 16) – it is our metabolic flexibility that has ensured human survival. I’d also say that there’s room for personal tastes and preferences.

[*This doesn’t mean we are well adapted to living on white bread and twinkies!]

However, I would argue that the notion that carbohydrates are not essential to optimal human health is a fallacy. Such claims are often made with reference to the Inuit diet (one of meat and fat, with essential zero vegetables/carbohydrates17) as “proof” of this idea. What is not commonly mentioned is the fact that the Inuit fared so poorly on such a carbohydrate-restrictive diet that their reproductive systems were compromised. Dr. Weston A. Price, as noted in his book Nutrition and Physical Degeneration, observed first-hand that the Inuit in fact supplemented their diets by liberal consumption of moose thyroid glands during the moose mating season (as a rich source of thyroid hormones which are needed for the conversion of cholesterol to sex hormones for fertility – impossible in a zero carbohydrate diet). Consequently, most of their children were born nine months after the moose mating season!

To me, anything that undermines our fundamental ability to survive as a species – ie reproduce – would indicate that it can’t possibly be compatible with optimal human health.

Question 3: What are the health risks of going low carb?

Apart from depleted sexual function as described rather explicitly above?!
I actually think there may be a time and place for short-term carbohydrate restriction in the management of some physical disorders and diseases (particularly seizure disorders and type II diabetes mellitus18). But the long-term effects of low carbohydrates diets seem to be pretty metabolically destructive (just as low-fat and low-protein diets are also destructive).

“A high-protein, low-carbohydrate diet drives insulin levels too low, thereby causing hypotension, fatigue, irritability, lack of mental clarity, loss of muscle mass, increased hunger, and rapid fat regain when carbohydrates are reintroduced into the diet. Not exactly a prescription for anti-aging.” Dr Barry Sears, author of The Zone Diet

Simply put, a lack of dietary carbohydrates causes a reliance on the production of glucose from non-carbohyrate sources (via gluconeogenesis), and subjects the body to increased amounts of pro-aging, pro-stress hormones (adrenalin and cortisol19). This long-term exposure to elevated stress hormones has a deleterious effect on human health, accelerating ageing and potentially leading to muscle wasting, demineralization of teeth and bone, impaired immune function, adrenal fatigue and decrease in sex hormones – all part of the stress response of the body. In addition to these problems, studies have shown that elevated cortisol levels over long periods have been associated android obesity20.

Low carbohydrate diets have been shown in the long run to inhibit thyroid function (possibly due to prolonged exposure to cortisol) thereby reducing metabolic rate, suppressing the conversion of T4 to the more metabolically active T3 hormone and increasing reverse T3 (not good). Incidentally, an underactive thyroid or ‘hypothyroidism’ (resulting in low metabolic rate) will instigate fat-gain, not fat-loss – good to know if you’re thinking of going low-carb under the impression it will cause you to lose weight (also see the note about cortisol, above).

Even the original potato-hater, Dr Atkins, admits in his book The New Diet Revolution that a low carbohydrate diet has the tendency to impact proper thyroid function, stating that “remember that prolonged dieting [in reference to the Atkins Diet] tends to shut down thyroid function. This is usually not a problem with the thyroid gland but with the liver, which fails to convert T4 into the more active thyroid principle, T3. The diagnosis is made on clinical grounds with the presence of fatigue, sluggishness, dry skin, coarse or falling hair, an elevation in cholesterol, or a low body temperature.”

These are my thoughts about extremely low carbohydrate diets, based on my observations, personal experience and research. Experiment for yourself, by all means, but watch out for increased pain, irritability/anxiety, cold fingers and toes, loss of appetite, thinning hair, reduced libido and other negative signs (and classic hypothyroid symptoms) that can occur when you don’t consume enough carbohydrates over the long term. You may just want to re-think this whole low-carb fad.

Oh yeah. And one more thing.

Of course, not all carbohydrates are created equal. Starchy plant organs and vegetables versus most cereal grains, particularly wheat, are like comparing night and day. But more on that to come… (UPDATE!! Read this post on grains!) 

 


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