Olivia Judson is a scientist and writer, whose columns in the New York Times leave me reading her quite often. Recently she posted about fat, the 40s, and long term brain degeneration.  No, not the most fun read, as my family is always thin until 30 and then we gain weight rapidly. It’s as if a thinness gene gets turned off.

Fat: the root of all nutritional evil?

But that isn’t what fascinated me deeply. One of her readers, one Mel Presley, of Roskilde Denmark, had this to say in response.

I want to suggest two possible roadblocks that obstruct the path to better understanding of the connections between obesity and cognitive decline.

First, what public health dogma advocates as a “healthy” lifestyle – a diet low in saturated fat (some would still say all fats) and plenty of prolonged, moderate-intensity exercise – is hardly natural for the human species. We’re omnivores, but without nutritional knowledge first available at mid-20th century, our energy, protein, and micronutrient requirements can only be met reliably by a mostly carnivorous diet that’s relatively high in animal fat. Prior to the dawn of agriculture 10,000 years ago, we didn’t have grains as a significant food source, and we certainly didn’t know that they had to be eaten with legumes to provide adequate protein quality. The natural human diet our ancestors followed the past 2 million years of our evolution was high in meat and animal fat, and usually low in carbohydrate unless a lucky find of fruit occasionally changed the picture.

The interesting thing is, if we disregard the modern paradigm of “healthy” eating and revert to our roots, we discover how nature designed hunger and starvation work. With a low carbohydrate intake and an ample supply of fatty meat, hunger abates and remains at bay even if we don’t eat for a few days. We live off our stored fat, depleting the fat depots that would otherwise accumulate and lead to obesity. If fruit begins to dominate the menu, the compelling, gut-wrenching sensation modern humans know as hunger takes over, and we’re driven to eat our fill of high-carbohydrate foods every few hours. In a primitive world, this makes sense, as it forces the body to accumulate the fat stores that saw our ancestors through times of famine. With a supermarket just around the corner, and Western fare full of grain products and sugar, the fat-storing “thrifty gene” has become our nemesis.

Primitive agrarian cultures modify the natural order by cultivating grain, beans, and starchy tubers, introducing high-carbohydrate energy sources, but growing these as crops without power equipment entails long hours of mostly low-intensity labor. Our 30-minute jog four times a week is a poor substitute for 12-hour days in the fields.

The second source of obfuscation in understanding how obesity and cognitive decline are related is the failure to understand that type 2 diabetes is not a condition one suddenly acquires by meeting arbitrary diagnostic criteria, rather, it is, in most cases, a latter stage of a degenerative process that begins with excess fat accumulation and other early signs of metabolic syndrome. Research that classifies subjects as non-diabetic and diabetic misses the emergence of a whole array of anomalies that can act independently and in concert to set the processes of degeneration in motion.

Increasingly as we age, an assured supply of inappropriate foods and, for most of us, a lack of compulsion to be physically active for long periods, make it easy for us to accumulate body fat while sparing us from having to endure the bouts of starvation needed to naturally deplete our fat stores. We develop insulin resistance as our fat stores make it more difficult for insulin’s action to pack in even more fat, so blood levels of glucose and insulin rise and stay abnormally elevated. LDL cholesterol particles become glycated, making them difficult for the liver to remove from the circulation, and we develop one form of dyslipidemia. If we persist in consuming a large carbohydrate intake, we develop elevated triglycerides and a shift toward small, dense LDL, other forms of dyslipidemia. The high insulin levels may provoke a type of cellular-level bloating in smooth muscle cells, making them hypersensitive to nerve impulses and leading to blood vessel constriction and hypertension. Elevated glucose can directly damage the kidneys, nerves, and the retina.

These processes can take hold long before conventional medicine formally classifies a patient as type 2 diabetic, and they don’t portend well for our vascular systems or the vital organs such as brain and heart dependent upon them.

Mainstream medicine can “cure” anyone of metabolic syndrome: you just go on an unpalatable, low-fat, super-hypocaloric diet and spend the rest of your life feeling constantly hungry, chilled, weak, irritable, and depressed. Needless to say, there are not many takers.

Periodic, short-term starvation in some form of intermittent fasting or near-fasting shows promise, but research never integrates it into a high-fat diet because the latter, which academic medicine still dismisses with shrieks of “Atkins!”, remains taboo. Unfortunately, a politically-correct “healthy” diet makes IF hard to tolerate, killing its appeal.

All of which must make the food, pharmaceutical, and medical industries very happy. You don’t want to solve something as big as the obesity epidemic and upset their gravy train.

Now within this comment are a pants load of assumptions, one of which I’m not sure is necessary. Isn’t what Mel is describing, about prehistoric eating, true regardless how our ancestors ate? That binge-starvation cycles are independent of what you binge on, whether it be meat, or fruit, or fields of tubers (wild onions, perhaps)? The point he’s trying to make is that hunger is set off-kilter by abundance, that plentiful food was not around (except for the rich) until the late 19th and early 20th centuries.

That’s something, that by virtue of my diet, I’ve come to believe. Hunger fails you when you’re in my condition. It’s not an accurate measure of when to eat or how much. So in order to live, I eat what I need to, not what I feel like eating. Also, the idea that metabolic instabilities are something that predate the label “type 2 diabetic” is also quite appealing. Again, Mel didn’t give references, and this is just a nicely pieced together story at this point. Mel could be a nutritional scientist or an angry type 2. But I will say this kind of thinking does resonate within the diabetic community, who tend to think the ADA has failed them, that medicine has failed them, that the system does not give a care, and that it is very poorly equipped for early diagnosis and intervention.

FnS.

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