Motorneuron
Member
- Joined
- Jan 29, 2021
- Messages
- 444
Is there anything that can increase the number and proliferation of mitochondria in all organs of the body? I didn't say to increase the mitochondrial efficiency, but the number. Thank you.
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Ketogenic diet decreases mitochondrial efficiency as glucose is severely compromised. This diet is a perfect precursor for the switch to lactate utilization/cancer state.Exercise increases mitochondria number/density.
Altitude adaptation.
So does ketogenic diet.
Red light is supposed to increase cytochrome c oxidase which is helpful. PUFA (polyunsaturated fatty acids) makes things much worse.Is there anything that can increase the number and proliferation of mitochondria in all organs of the body? I didn't say to increase the mitochondrial efficiency, but the number. Thank you.
Uh, no, not from my personal experience. Lactic acidosis is very dangerous. This is not the same thing as getting a little sore after exercise which goes away pretty quickly.In any case lactate phobia is straw man fallacy.
Thanks for the mention, very helpful. Brook's summary article is at https://www.cell.com/cell-metabolism/comments/S1550-4131(18)30186-4In 1970s physiologist George Brooks discovered the lactate shuttle by which lactate generated in one muscle type is directly utilized in the other without liver restoration to glucose.
I thought that the ketogenic diet depleted deuterium which in turn boosts the mitochondria?Ketogenic diet decreases mitochondrial efficiency as glucose is severely compromised. This diet is a perfect precursor for the switch to lactate utilization/cancer state.
Thyroid hormones cause mitochondriogenesis. I briefly tried a ketogenic diet 7 years ago and could feel the IQ points marching out through my ears to find a safer, peatier host.
The Role of a Mitochondrial Progesterone Receptor (PR-M) in Progesterone ActionThere is evidence that cold therapy improves mitochondrial health through a process known as “mitochondrial biogenesis,” or in other words, by producing more of them. Cold therapy can be compelling because it forces you to become comfortable with discomfort. It is as much mental training as a physiological one
"UCP1 [uncoupling protein 1] is highly expressed in BAT [brown adipose tissue] that classically was thought to be found only in newborns, but persists in adults. BAT is located in the neck, thorax, and abdomen; is more frequent in females compared with males; inversely correlates with age and BMI; and is induced by cold stimulus.53 UCP1 is also expressed in beige or brite (combination of letters from brown and white) adipose cells that are induced from progenitor cells within white adipose tissue (WAT) by several factors, including fibroblast growth factor 21, parathyroid related protein, irisin, and meteorin-like hormone.54 Compared with WAT, BAT and beige adipocytes have a much higher mitochondrial content and oxygen consumption55
. . .
BAT and beige adipocyte activity is stimulated by cold via neural control of the sympathetic nervous system, linking central control of NST [non-shivering thermogenesis].59 Activity is also regulated by circulating catecholamines via β-adrenergic receptors60 and thyroid hormone with enhancement of mitochondrial biogenesis and UCP1 expression.60 Even though the quantity of BAT is low in adults, there is evidence of control of BMR and thermogenesis related to cold and food intake. In animal studies, experimentally induced BAT deficiency results in obesity with decreased MR.61
. . .
Progesterone increases β-adrenergic receptor expression and catecholamine-induced lipolysis.64 In addition, progesterone induces expression of PPARγ65 and UCP1 in adipose tissue,66 thus positively regulating mitochondrial biogenesis. The role of PR-M [non-genomic, truncated "mitochondrial progesterone receptor"] in BAT remains to be investigated. Theoretically, a progesterone induced increase in BAT cellular respiration could result in greater NST via PR-M action"
In more ways than one!"Taking about 10 milligrams of progesterone had a very soothing effect, but if I kept it up for about a week, it was like I was constantly getting out of a cold shower."
- Ray Peat, "Your Own Health And Fitness Heart Brain Cancer and Hormones", July 29 2014
I can't comment as to that but I can say that it was proven almost 100 yrs ago that compromised mitochondrial function, at least as far as it's ability to utilize glucose, it's preferred energy source, causes the mitochondria to switch to lactate which is about 25% the efficiency of glucose which, in turn, promotes rapid cellular division to try recover energy of the "afflicted" region which becomes your tumor.I thought that the ketogenic diet depleted deuterium which in turn boosts the mitochondria?
Love studies as they lack real world experience. Gave up on the "numbers" & studies when I found my best path. My point about keto is for couch surfers is that they don't have heavy energy requirements &, as such, can coast through this lifestyle. I lift heavier than most & 6 days a week & keto just doesn't cut it. Significantly reduced rep capacity & set duration, depletion of muscle strength & it's associated mass. There is a direct correlation to available serum testosterone levels & the drastic rise in cortisol when said test is consumed under physical duress & this reduction in test/surge in cortisol will happen for me within 20 or so minutes on keto as opposed to 45 minutes on glucose fueled lifting.Couch potatoes don't have much keto and don't need much. Endurance athletes do.
>Significant amounts of ketone bodies are also produced during a non-ketogenic diet, leading to blood levels of around 0.05 mmol/l for acetoacetate, 0.05–0.4 mmol/l for βOHB, and 0.02–0.05 mmol/l for acetone. The levels vary over the day, decreasing with the uptake of carbohydrates and increasing in periods between meals or because of prolonged muscle work. In metabolic healthy persons, systemic concentrations of ketone bodies may reach 5–7 mmol/l, after prolonged fasting, or up to 5 mmol/l during a ketogenic diet (Table 1). However, the buffering power available during a healthy metabolic state is able to cope with such amounts of ketotic acids and a normal pH of the blood is maintained. Higher levels of circulating ketone bodies do not occur during starvation because fasting blood insulin levels remain in the low normal range which is sufficient to prevent an unrestricted increase of lipolysis.