Not enough protein - what will happen?

[Motif]

What symptoms would one get?

Or do you have experience with low protein symptoms?

 

[Rafael Lao Wai]

Muscle loss and a hunger which cannot be satisfied

 

[Blaze]

What symptoms would one get?

Or do you have experience with low protein symptoms?

Like anything in this life it will depend on a number of different variables. If you have a low protein diet but are not hypocaloric and still get enough calories from sugar or fat, the body can surprisingly thrive for quite a while on a diet with as little as 5% protein.
If you try this low protein thing without getting around 2500 calories a day , the hypocaloric state will raise cortisol and you will canabalize your body tissues and shrink your fat stores and muscles and lastly your organs to survive.

The real question would be why would you even try this type of low protein diet. I would only recommend a protein restrictive diet in an extreme disease states like CKD or maybe runaway cancer growth , and even then never coupled with calorie restriction. (On a side note, that T Colin Cambell guy claimed to have turned on and off tumor growth just by going between 5% and 20% protein intake)

Anyway, to answer your question, if you get the calories you need , you might be surprised and have absolutely no symptoms at all even with a super low 5% or 10% protein diet.

There was a guy in Scotland in the 1960’s I think was named Angus or something like that ,who didn’t even eat for a whole year and was not suffering any lack of protein syndrome. He was severly overweight and his body got what it needed for a whole year living off his stored fat and amino acids. A thin guy would never be able to get away with that, though.

Everthing you do to your body should have a goal in mind. What do you want to accomplish with a very low protein diet or was the question just theoretical in nature merely to satisfy a momentary curiosity?

 

[Sefton10]

Anyway, to answer your question, if you get the calories you need , you might be surprised and have absolutely no symptoms at all even with a super low 5% or 10% protein diet.

The last few days I’ve been eating lower protein than usual. Say 90-100g rather than 150g+. I actually feel much more metabolic than usual, with very warm temps. I’ve kept the cals up by just eating more fruit and cheese/chocolate. Going to keep this up for a while and see if any craving for more protein kicks in.

 

[Marcine]

You won't convert much T4 to T3 so your muscles will suffer and no retinol is a bad idea although I suppose you could supplement. I don't get why anyone wants to limit protein. It's why poor countries suffer from malnutrition. You should at least eat fish, eggs, offal and shellfish if you want to eat less animal meat.

 

[nomoreketones]

hunger which cannot be satisfied

Yup. You can tell if you have protein hunger when you are starving and you eat a bunch of bananas and feel just as hungry,.

 

[LA]

this:

Muscle loss and a hunger which cannot be satisfied

also - Pain, stiffness, grumpy, thinning hair, blurry vision

 

[Motif]

But how much is enough is the question.

im muscular, but have lots of issues, but I don’t think low protein is causing this.

it’s my low zinc / copper and whatever causes them to stay low. Gut , digestion or whatever

 

[nomoreketones]

But how much is enough is the question.

im muscular, but have lots of issues, but I don’t think low protein is causing this.

it’s my low zinc / copper and whatever causes them to stay low. Gut , digestion or whatever

Cut back on protein and see what happens. I think protein requirements are different for everyone.

 

[LA]

But how much is enough is the question.

im muscular, but have lots of issues, but I don’t think low protein is causing this.

it’s my low zinc / copper and whatever causes them to stay low. Gut , digestion or whatever

try different foods and see if anything helps your mineral issues and any other issues. Also stop some foods. Take notes and be your own Guinea Pig. Everyone is different the safest guidance is to study what the healthiest of your ancestors ate, parents and their siblings, grands and their siblings, great-grands and their siblings, great-great-grands and their siblings.

 

[Amazoniac]

- Kwashiorkor: more hypothesis testing is needed to understand the aetiology of oedema

Spoiler

"The aetiology of kwashioror is truly not known. Most frequently, diets that are based on maize, cassava or rice are associated with kwashiorkor. (3) Kwashiorkor is not the result of prolonged breastfeeding, and neither deficiency in protein intake nor low levels of antioxidants in the diet are considered primary causal factors of kwashiorkor as the diet of children with marasmus have similar deficiencies. (4) Higher levels of aflatoxins have been found in the serum and liver of children wirh kwashiorkor than in marasmus. (5) Hypotheses have been advanced over the last 100 years suggesting that protein deficiency, hypoalbuminemia, and excessive oxidant stress cause kwashiorkor. Evidence associating these aetiologies with kwashiorkor have been cited, however dietary supplements of protein and antioxidants in children who are high risk for kwashiorkor have not been shown to reduce the risk of kwashiorkor (6), and oedema resolves on a restricted protein diet. (7) Aflatoxin intoxication has been advanced as an aetiology of kwashiokor, but kwashiorkor is seen in populations without evidence of ingestion of aflatoxin and this is not supported by studies of post-mortem tissues (8). Other social and economic risk factors include recent cessation of breastfeeding, recent infection, high birth order, incomplete immunization, and disruptions in the child's caretaker's status such as parental death, not living with a parent, unmarried caretaker, young age of mother, living in a temporary home, or parents not owning land. Recent measles infection has been found as a risk factor for the development of kwashiorkor, many caretakers report diarrhea as a precipitating factor in kwashiorkor."

"A potential mechanism by which peripheral oedema occurs in kwashiorkor may well be related to release of water that is normally bound to glycosaminoglycans. Glycosaminoglycans are long polysaccharides consisting of a repeating sulphated carbohydrate units, bound to short protein core in all connective tissues and basement membranes of the bodv. Glycosaminoglycans contain moieties that are subject to oxidation/reduction, and they bind water avidly through cohesive forces of “structured water” similar to that found in a gel. Recent studies show that children in kwashiorkor have abnormal renal architecture that can be explained by loss of glycoseaminoglycans (10) and they lose glycosaminoglycans from the intestine (11) (particularly heparan sulfate proteoglycan); the loss of the ability of glycosaminoglycans to retain water in the form of a gel, may cause the appearance of pitting oedema."

"Apart from mechanisms that disrupt glycosaminoglycans or alter the redox (oxidation/reduction) state of the cells, there are other putative etiologies that require examination.

First, the development of kwashiorkor occurs only when the diet provides marginal amounts of macro- and micronutrients, but inadequate dietary intake of those essential nutrients so far examined is not a sufficient to damage cell membranes resulting in generalized oedema. Another interacting, coincident environmental factor must play an important role in the pathogenesis of kwashiorkor. The gut flora constitute a relatively uncontrolled metabolic system capable of synthesizing noxious and beneficial compounds and altering the dietary constituents. Populations of gut flora change with change with diet and physiological state. (12) The gut microbiota can work synergistically or antagonistically with the human host as they metabolically consume and process nutrients. (13) The gut microbiota have been shown to render some dietary toxins innoxious (14), but also to nrodiirr. toxic meraholitps rannhle of rtamacrinrr rl-ip ht-qin liver or kidney. (15) The 1014 bacteria present in the human intestine produce metabolites which may exert a potent effect on the human host. Perhaps kwashiorkor is the result of changes in the gut microbiota that favor the production of metabolites that insult the human cell membrane integrity in an undernourished host, or disruption of the gut microbiota's protective function with respect to environmental toxins.

A second hypothesis is that a change in vanadium metabolism, either through a dietary deficiency or an alteration in the chemical form of the metal, may cause the sodium retention characteristic of kwashiorkor. (16,17) Vanadate is a very potent inhibitor of the sodium pump at physiological concentrations. The sodium pump is responsible not only for transport across cell membranes but also for the reabsorption of sodium from the kidney. Failure to inhibit the reabsorption of sodium either because of a vanadium deficiency or conversion of vanadate to the inactive vanadyl ion could lead to salt and water retention and thus to edema formation. The serum levels of vanadium are low in kwashiorkor. (18)

Third, although kwashiorkor has not been prevented with an antioxidant cocktail (6), there is consistent evidence of oxidative stress in these children, with low levels of antioxidants, and elevated levels of pro-oxidants in the blood. Survival is improved if sulphur containing antioxidants are given during treatment. (19) The metabolites of these nutrients particularly, selenium and sulfur, are responsible for maintaining the redox level in the cells. The intracellular environment is much more oxidized than normal (20) which would account for the pathological features of kwashiorkor (membrane damage, fatty liver, skin lesions) and may be one mechanism whereby glycosaminoglycans are lost, the valences of vanadium are changed and the metabolites coming from small bowel bacteria exert their toxic effects.

However, without determining the precise etiology and pathogenesis of kwashiorkor we are not in a position to formulate rational or effective prevention strategies. This is important, because, unlike marasmus, there is no “moderate” or “mild” kwashiorkor whereby we can recognize the condition in its early stages and prevent deterioration to a stage when the condition is often lethal."