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Last week we took a look at one of the papers that Wikipedia has as a reference for its article on starvation mode. We also learned about the metabolic phases of starvation, the stages our body goes through when experiencing a complete cutoff of food supply. This week we’ll go over the other papers that are referenced in Wikipedia’s page, and, if anything interesting turns up, we’ll add it to the starvation mode mythos.
Second paper: Elia M (December 2000). “Hunger disease”. Clin Nutr. 19 (6): 379–86. This paper is a sobering one, considering that it begins by talking about famines (hunger disease), and the portrayal of them throughout history. Fortunately, the paper cheers up as it goes on into the findings of autopsies carried out on humans and other animals that died of starvation. Unsurprisingly, considering last week’s post, the general rule is that such cadavers display almost no fat reserves, as well as a loss of 25-50% of lean tissues and organs. The implication of this is that the consumption of the body’s stores of fat and protein during starvation is regulated so that survival is prolonged. In other words, fat deposits not only store energy, but a greater amount of them means that their oxydation can be carried out in such a way that more protein is preserved at their expense. In plain english: an obese individual will outlive a non-obese one during starvation both because of larger energy reserves, and because their muscles and lean tissues will be used as fuel to a lesser extent.
The paper then goes on into how the kidneys are also involved in neoglucogenesis, and how their role becomes greater as starvation is prolonged. Furthermore, obese individuals tend to involve their kidneys as much as their livers for neoglucogenesis, perhaps even producing more glucose with the former than the latter. So it seems that obese individuals and lean ones experience starvation in different ways. Straight from the paper:
All these observations suggest that it is no longer acceptable to consider the metabolic response to starvation as stereotyped. Many textbook descriptions of the biochemistry of human starvation are based on observations made in obese individuals, which do not necessarily apply to lean individuals.
This is quite interesting, and it’s something that I’ll have to keep on the back burner as this blog’s content grows. Anyhow, on to the next paper.
Third paper: Swaner, JC; Connor, WE (Aug 1975). “Hypercholesterolemia of total starvation: its mechanism via tissue mobilization of cholesterol”. The American Journal of Physiology. 229 (2): 365–9. I have to admit I loved this paper. The previous ones were mostly reviews: they presented the state of the art at the time, but they didn’t truly provide their own hypotheses, results or discussion of said results. This paper, on the other hand, does just that. Let’s go over the basic idea: Total caloric starvation in some animals is accompanied by an increase in the levels of plasma cholesterol (hypercholesterolemia), and two possible explanations are proposed:
- cholesterol synthesis keeps going on despite a lack of intestinal excretions
- due to starvation, the body mobilizes and consumes tissues that also contain cholesterol
Now, some additional information is needed to make sense of what we’ve just said. Cholesterol is one of those organic molecules with lots of uses: it’s a component of animal cell membranes, and it’s also a precursor for the synthesis of vitamin D, steroids, and bile. Due to its importance, cholesterol is synthesized by the body in the liver (that magical, do it all organ), in the intestines, and it can also be ingested. There will be more to be said about cholesterol in future blog posts, so let’s leave it at that for now. The point of the paper is that, because cholesterol is a component of fat cells, and fat cells are mobilized and used as energy sources during starvation, then the increase in plasma cholesterol might reflect the mobilization of such fat reserves.
The rest of the paper goes into how the experiments to test this hypothesis were carried out. It is a simple, short and easy to understand paper, so I’d recommend it if you’re interested in getting to know the structure and content of a standard scientific paper. Anyway, the paper concludes that:
These results support the hypothesis that cholesterol stored in the lipid droplet of the adipose tissue cell is released into plasma and is the chief source of the hypercholesterolemia observed during complete caloric starvation.
Having said all that, let’s close the starvation mode “episodes” of this blog. There is such a thing as a starvation mode / starvation response. It is not, however, this nebulous thing that stops your metabolism going, or keeps it so slow that whatever you eat gets added to your fat. The reality is that metabolism keeps going, albeit with some changes, and the source of energy is what changes, like a hybrid car on the road switching from its battery to its engine. Starvation mode is simply a series of mechanisms that our body follows when its food supply is cut short in order to extend our survival.
Now, starvation mode is the gateway drug to other misconceptions on weight loss, weight gain, nutrition, and health, so it had to be dealt with. Next week post we will deal with metabolic damage.
See you next week! If you liked this post and would like to see similar material, please visit the Rebuttals to Fatlogic section of the blog.