From what I gather, it’s been difficult to pinpoint the role of plants in the diet of our ancestors for a variety of reasons. For example, evidence of plants on cooking tools and dental remains is suggestive but doesn’t disprove the possibility that said evidence came from preparing the plants for some other purpose (eg, tools, weapons, or medicine), or that the stomach contents of an herbivore was ingested (which gets partial credit).
That said, after reviewing a few studies on the topic (see below), it’s safe to say that plants were eaten, probably frequently, and the types & quantities varied seasonally & geographically. Collectively, the data suggest we aren’t carnivores.
@CaloriesProper I do wonder why there is so much debate around this? Ancient humans ate plants and animals. The end.
The original lipid hypothesis stated, more or less, that lowering blood cholesterol would reduce premature mortality from heart disease. At the time, it was thought that dietary cholesterol and saturated fat increased the ‘bad’ type of blood cholesterol, so the advice was to restrict those foods. All of that was wrong.
About a decade ago, Michael Brownlee posited that AGEs were one of The Four Horsemen responsible for the microvascular complications of diabetes.
Thereafter, the image below (or a closely related one) appeared in at least one talk at every major diabetes conference for about 5 years. Then it faded – maybe not because it is wrong, but rather just too simplistic to be useful (similar to CICO & ELMM).
“A diet rich in processed foods and fat – and the extra weight that comes along with it – may actually cause fatigue, a lack of motivation and decreased performance, according to a recent study involving lab rats… excessive consumption of processed and fat-rich foods affects our motivation as well as our overall health.”
(this is categorically false as both diets used in the study being discussed were very low in fat.)
The theory itself isn’t too far-fetched: a crap diet can cause weight gain and reduced energy expenditure, or a tendency to minimize any kind of physical activity… instead of: “’laziness’ causes obesity.” And whether or not it’s true, unlike what some would have you believe, this wasn’t the study to prove it.
Nutritional ketosis is a normal, physiological response to carbohydrate and energy restriction. A ketogenic diet is an effective weight loss strategy for many. Ketoacidosis, on the other hand, is a pathological condition caused by insulin deficiency. The common theme is low insulin; however, in ketoacidosis, blood glucose levels are very high. Ketone levels are elevated in both states, although are 10-20x higher in ketoacidosis (~0.5-2 vs. > 20 mM). Nutritional ketosis and ketoacidosis should not be confused with one another, and a ketogenic diet doesn’t cause ketoacidosis.
In ketoacidosis, gluconeogenesis occurs at a very high rate and the lack of insulin prevents glucose disposal in peripheral tissues. Skeletal muscle protein breakdown contributes gluconeogenic substrates, exacerbating the problem. This can cause blood glucose to reach pathological levels, exceeding 250 mg/dL.
More from T.S. Wiley and Dr. Kruse on seasonal eating in what appears to be the primary model for its justification for use in humans – hibernating mammals.
How it goes, or so they say: in summer, hibernators massively overeat, including carb-rich foods, in order to generate muscle and liver insulin resistance, so as to promote body fat growth. The long light cycle reduces evening melatonin, which pushes back the usual nighttime peak in prolactin, which causes an abnormal resistance to leptin, which induces hypothalamic NPY and subsequent carbohydrate craving. Ergo, summer is fattening. In today’s day, increased artificial lights guarantee year-round pseudo-summer; and we no longer experience the benefits of the short light cycle: longer sleep times (akin to hibernation) and fasting – either complete fasting as in hibernation, or pseudo-fasting, ie, a ketogenic diet.
Hat tip to Jane Plain and her ongoing series on “The physiology of body fat regulation” for citing this study as it provides a rather interesting insight into the psychoendoneuropathophysiology of the obese condition. Eating in the Absence of Hunger.
In the original article, Taubes basically re-states his philosophy on obesity. Nothing new. But one rebuttal by Cottrell got under my skin (Cottrell, 2013), and Taubes’ response was woefully inadequate.
Cottrell [sic]: “A third incorrect assertion is that obesity can be attributed to the conversion of carbohydrate to fat. This is an unsatisfactory explanation of obesity, because this route is a minor pathway to depot fat in humans, even under conditions of substantial overfeeding of sugars to obese subjects. An unproved assumption is that the hypothetical diversion of carbohydrate energy into fat storage leaves the subject hungry, thus stimulating overeating.”
Cottrell set up a straw man and handily took it down. The primary mechanism whereby excess carbs contribute to obesity is via insulin’s effects on adipose tissue. Even if you’re eating very little fat, insulin will cause it to get stored. Insulin is very good at this – it is actually far more potent at stimulating fat storage than it is at stimulating glucose uptake (eg, Insulin vs. fat metabolism FTW). Cottrell’s straw man is that excess carbs themselves are stored as fat. This does not occur to any appreciable extent in humans. Here is why I believe that to be true, from one of most insightful and informative studies on the topic IMHO.