One of the problems I am currently trying to deal with is the crumbling concept of calorie restriction as a means to health and longevity when it is confronted by the following proposition: In biology, ENERGY and STRUCTURE are powerfully interdependent. Sounds Blakeian and Ray Peat, who has made the propositon his leitmotiv, is something of a Blake scholar. According to Peat it is the dissipation of energy in a faulty structure which leads to health problems: under such conditions the more energy the more problems. He identifies several structure disruptive substances (PUFA, iron, estrogen,) which if consumed sufficiently cumulate in the organism and pose a serious oxidative threat and are powerfully endocrine disruptive. There are also certain mechanisms which relate to energy production such as glycolysis, lipolysis and lipid oxidation which are less effective than glucose oxidation, the ideal less wasteful, less mitochondria damaging way of producing cellular energy. His evidence for this is very compelling, he draws from decades of scientific studies and experience. CR is mentioned several times in his newsletters in a positive light, but as far as I am aware, he never confronts it directly with his principal axiom.
Calorie restriction over time clearly shrinks the biological structure: this is most dramatically exemplified by the shrunken bone mass of most long term (over 4 years?)practicants. If under these condition CR leads to health and longevity it must be beacause energy is dissipated in a smaller simplified structure where the potential for disruption is reduced. Does it necessarily follow that energy wastage is minimized with CR and that all energy derived from food is efficiently used? According to Peat to metabolize efficiently is to metabolize fast. According to current theory, CR slows aging by slowing metabolism and thus achieves one of its pricipal effects by slowing the rate and extent of oxidative reaction (production of ROS) which unhindered lead to accelerated aging according to the free radical theory of aging. I have posted on the CR list a pair of compelling recent studies with commentary which challenge the notion that a rapid metabolic rate leads to accerlerated aging: admitedly the living organism is not a closed energy system and the rate of aging does not depend upon using up a limited energy supply in the sense that the faster it is used up the sooner the organism dies. Yet nor can it mean that its parts ware out sooner since the ability to metabolize fast is dependant by its nature on the efficient functioning of these parts, that is, a fast metabolic rate is impossible to maintain when the organism is on its way to waring itself out through increasing oxidative damage. In aging everything slows down. A fast metabolism is thus necessarily a biologically young metabolism which is capable of controling damage through efficient repair. No way around this logic. Pigeons are very fast metabolizers, yet can live up to 35 years. Metabolism would seem to be no reliable predictor of lifespan and aging to depend upon other factors than metabolism which seems more to be specie specific.
Metabolic rate is something none the less subject to impairment, though not, as said, as a function of its efficiency. Hypothyroidism is classically synonymous with slow metabolism. The organism is sluggish and energy production is inneficient and wasteful. Extremities are cold. Slowing down metabolism as a way of controling aging is a huge misunderstanding. It would seem more likely that controlling the factors which impair metabolism and which damage the cellular respiratory structure which insures efficient metabolism would slow down aging. Peat cites the experiments in which essential fatty acid deficient rats become fast metabolizers implying that these animals had hindered metabilism through consumption of PUFA from their standard feed. Under such conditions symptoms of malnutrition develop quickly as nutrients are more rapidly used up. These rats just need better food and more calories. If CR leads to slow metabolism as many would have it, the effort to obtain optimal nutrition would likely be superfluous as nutrients would not be used up but eliminated. Low T3 were interpreted as indicators of a slow metabolic rate (Fontana) in a recent human CR study and made to confirm the theory that a slow metabolic rate is an effect of CR. I do not know whether the subjects actually underwent testing of metabolic rate. Lower body temperature typical of long term CR practicants are an indicator of low metabolic rates. The tendency of long term CRers to put on weight by the slightest increase in daily calories seem indicative of slow metabolism. With rapid metabolism there would be no such increases in weight. In another experiment rats very succeptible to type 2 diabetes were cured by EFA deficiency. They also became high metabolizers. Are PUFA endocrine disruptive? Do high levels of tissue PUFA lead to greater oxidation, impair mitochondria respiration? and lead to slow metabolism? It has also not escaped the notice of experimentors that EFA deficient cells are much more resistent to toxic chock than non deficient cells.
This opens the way to thinking that the consumption of more calories under permissive conditions would lead to a more complex, more resistant, more longevous and intelligent structure.