protective inhibition

[Blossom]

From The GABA system,defenses, and tissue renewal May 2008 newsletter

The agents of protective inhibition increase survival, along with the mental abilities and metabolic rate. Too often the excitants suppress energy production while increasing the need for energy, leading to impaired functions and failure of restorative processes.

 

[Amazoniac]

⮣ Getting enough energy for immunity
⮣ Counting Calories: The Cost of Inflammation
- Energetic trade-offs and hypometabolic states promote disease tolerance

 

[Blossom]

⮣ Getting enough energy for immunity
⮣ Counting Calories: The Cost of Inflammation
- Energetic trade-offs and hypometabolic states promote disease tolerance

Thank you for these interesting articles.

 

[Amazoniac]

- Trade-offs in evolutionary immunology: Just what is the cost of immunity?

Spoiler

"Macrophages, like other immune cells, are nutrient-demanding cells as evidenced by their hypermetabolic state and significant rates of glucose and glutamine utilisation relative to other cells in the host. Based on in vitro O2-consumption rates, elicited macrophages turn over ATP in the cell 10 times per minute, almost comparable to maximally functioning heart muscle (Newsholme and Newsholme 1989). Thus, immunity demands fuel in terms of nutrients and energy at remarkable levels, which reflects the evolutionary importance that has been placed on ensuring host survival."

"General statements about the metabolic costs of immunity to the whole organism are difficult to assess during an immune challenge. Severity, type, and duration of infection, ambient temperature, and gender, age, and nutritional status of the host all influence the cost of mounting an immune response. However, it is clear from selected studies with humans and laboratory animals that even mild up-regulation of the immune system can be costly metabolically to the host."

"Unlike starvation where the host eventually adjusts physiologically to the reduction of nutrient inputs by decreasing metabolism, infection leads to a hypermetabolic state to support the up-regulation of the immune system (Table 1). Isolated mitochondria of laboratory rats stimulated in vivo with TNF-a or IL-1 can undergo a 30% increase in respiration rate (Jin et al. 1995). Infusions of IL-6 into healthy volunteers will increase resting metabolic rates by 25% (Tsigos et al. 1997). To fuel this up-regulation, immune cells require glucose and glutamine at high levels (Crouser and Dorinsky 1996), which leads to the rapid breakdown of the body’s reserves of protein (to provide glutamine), carbohydrates, and lipids (Michie 1996). Moderate infections can easily lead to 150–200% increases in rates of gluconeogenesis in the host, often leading to severe wasting of lean tissue if such infections chronically persist. Animals typically become insulin-resistant as an adaptation to insure glucose concentrations in circulation remain high for the insulin-independent immune cells involved in wound healing and combating infection (Chiolero et al. 1997)."

"An unfortunate consequence of fighting an infection in nearly all species examined is a reduction in feed intake. This sepsis-induced anorexia is striking in the sense that it occurs at a time when the body needs an influx of nutrients to support the increased demands of mounting an immune response (Scrimshaw 1991). Reduced feed intake appears even with rather mild immune challenges such as those associated with simple vaccination (Gandra and Scrimshaw 1961). Consequently, catabolic processes must activate to support the additional fuel requirements of immune cells and protein synthesis (acute-phase proteins, antibodies). Kyriazakis et al. (1998) forward two hypotheses to explain the occurrence of anorexia during sepsis that are consistent with observations during infection. One hypothesis states that the reduced food intake promotes an effective immune response, while the other (non-exclusive?) one asserts that anorexia allows the animal to be more selective in its diet to reduce the risk of further infection."

"Malabsorption also can accompany infections leading to additional nutritional constraints on the host. A combination of factors contribute to this syndrome, including physical blockage of absorption sites by bacterial overgrowth in the gut, alterations in villus structure, reductions in transit time such as with diarrhoea, and reductions in blood flow to the gut."

 

[gaze]

"Unlike starvation where the host eventually adjusts physiologically to the reduction of nutrient inputs by decreasing metabolism, infection leads to a hypermetabolic state to support the up-regulation of the immune system (Table 1). Isolated mitochondria of laboratory rats stimulated in vivo with TNF-a or IL-1 can undergo a 30% increase in respiration rate (Jin et al. 1995). Infusions of IL-6 into healthy volunteers will increase resting metabolic rates by 25% (Tsigos et al. 1997). To fuel this up-regulation, immune cells require glucose and glutamine at high levels (Crouser and Dorinsky 1996), which leads to the rapid breakdown of the body’s reserves of protein (to provide glutamine), carbohydrates, and lipids (Michie 1996). Moderate infections can easily lead to 150–200% increases in rates of gluconeogenesis in the host, often leading to severe wasting of lean tissue if such infections chronically persist. Animals typically become insulin-resistant as an adaptation to insure glucose concentrations in circulation remain high for the insulin-independent immune cells involved in wound healing and combating infection (Chiolero et al. 1997)."​

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what is the best thing to do in this scenario? up the fats to get more calories in, or lower fats to improve insulin sensitivity? high dose minerals, specially magnesium? more or less protein? the lowered appetite makes all of the options difficult in certain ways

 

[Sefton10]

A couple of sections I highlighted recently in Rory Sutherland’s book, Alchemy.