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Insulin stimulates the release of vitamin A stores from the liver (Bowles, 1967)

#1 · October 15, 2023, 8:57 am

Bowles WH. Influence of insulin on liver vitamin A in rats. Diabetes 1967; 16:704-707.

https://www.jstage.jst.go.jp/article/jcbn1986/11/1/11_1_47/_pdf

Bowles [4] showed that injection of insulin causes an increased rate of depletion of vitamin A in the liver in nondiabetic rats.

This could explain why so many people here on a low vA diet (inadvertently often also a higher carb diet) see their serum vA levels increase.

The increasing insulin levels needed to regulate glucose is also causing the increased release of vA from the liver.

Therefore, the susceptibility for the vA detox setback will also be proportional to the extent a person is pre-diabetic, or even diabetic.

Thus, why, (as far as I know) there are not a lot of reports of a serious detox setback when taking on the carnivore diet.

Thoughts?

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#2 · October 15, 2023, 9:38 am

Cita de genereux el 15 de octubre de 2023 a las 8:57

La insulina estimula la liberación de las reservas de vitamina A del hígado (Bowles, 1967)

Bowles WH. Influencia de la insulina sobre la vitamina A del hígado en ratas. Diabetes 1967; 16:704-707.

https://www.jstage.jst.go.jp/article/jcbn1986/11/1/11_1_47/_pdf

Bowles [4] demostró que la inyección de insulina provoca una mayor tasa de agotación de la vitamina A en el hígado en ratas no diabéticas.

Esto podría explicar por qué tantas personas aquí con una dieta baja en va (sin darse cuenta, también una dieta alta en carbohidratos) ven aumentar sus niveles séricos de va.

El aumento de los niveles de insulina necesarios para regular la glucosa también está provocando una mayor liberación de va desde el hígado.

Por lo tanto, la susceptibilidad al retroceso de la desintoxicación también será proporcional al grado en que una persona sea prediabética o incluso diabética.

Por lo tanto, (hasta donde yo sé) no hay muchos informes de un revés grave en la desintoxicación al seguir la dieta carnívora.

¿pensam?

So why didn't the sugar and rice Kempe diet have that poisoning setback and cure people with diabetes

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#3 · October 15, 2023, 12:16 pm

Hi @el,

That's an excellent question. I don't have an answer, but can only speculate that being extremely low in protein was a key factor in not mobilizing vA from the liver.

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#4 · October 15, 2023, 1:16 pm

From my history,

I have been on high carb/high fat/low protein diet and didn't have issues until I added protein into my diet in a considerable amount. I got down to 138lbs on this diet.

I have also been on a high protein/high fat/low carb diet and did ok until I added carbs back in.

I wonder if a moderate fat/moderate protein/lower carb diet would be ideal. Going low protein long term probably isn't the wisest route and having too many carbs would spike insulin too frequently.

#5 · October 15, 2023, 3:25 pm

Quote from ggenereux on October 15, 2023, 8:57 am

Insulin stimulates the release of vitamin A stores from the liver (Bowles, 1967)

Bowles WH. Influence of insulin on liver vitamin A in rats. Diabetes 1967; 16:704-707.

https://www.jstage.jst.go.jp/article/jcbn1986/11/1/11_1_47/_pdf

Bowles [4] showed that injection of insulin causes an increased rate of depletion of vitamin A in the liver in nondiabetic rats.

This could explain why so many people here on a low vA diet (inadvertently often also a higher carb diet) see their serum vA levels increase.

The increasing insulin levels needed to regulate glucose is also causing the increased release of vA from the liver.

Therefore, the susceptibility for the vA detox setback will also be proportional to the extent a person is pre-diabetic, or even diabetic.

Thus, why, (as far as I know) there are not a lot of reports of a serious detox setback when taking on the carnivore diet.

Thoughts?

Any chance that the increase in insulin causes the liver to release/transport retinol for peripheral storage in adipose tissue?

What if the effect of sending retinol for storage during weight gain and and recalling retinol from storage during weight loss causes hiccups along the way?

Losing fat for me increases my symptoms for sure and seems to be worse when protein is in excess.

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#6 · October 16, 2023, 11:41 am

Quote from wavygravygadzooks on October 16, 2023, 11:41 am
It's a shame they never seem to look for Vitamin A in other tissues in these studies, and seldom do they look at Vitamin A in the feces and urine. My big question is always, where did it actually go?! It seems like a stretch to assume it is always fully excreted from the body.

Something of note in the study Grant posted is that the authors attributed the final amount of Vitamin A in the liver directly to food consumption. However, the control group was reported to consume 68% and 74% of the food that diabetic and diabetic + insulin groups consumed, respectively (during the last 3 weeks of the study...we need to know what it was for the entire study to get a full comparison of Vitamin A intake though), whereas the final liver Vitamin A level in the the control group was 62% and 57% of diabetic and diabetic + insulin groups, respectively. That suggests a disproportionate accumulation of Vitamin A in the livers of insulin-treated rats who ate 36% more food than controls but had 76% more Vitamin A stored in their livers than controls.

On the other hand, in a study cited within the one Grant posted, diabetic rats treated with insulin had less Vitamin A stored in the liver than controls after a period of explicit Vitamin A supplementation. Not sure how to make sense of those apparently disparate results (different amounts or forms of insulin, or different affects of the toxin that was used to make the animals "diabetic"?).

Of interest in this latter study, all animals that were supplemented with Vitamin A and which subsequently underwent a Vitamin A "depletion" period appear to have lost a minimum of half their liver stores within only 12 days! Animals injected with insulin lost far more than controls. It's hard to believe all that Vitamin A was excreted from the body so quickly. For some reason, virtually all of the study groups gained weight during both the Vitamin A supplementation period and during the "depletion" period that followed (maybe because they were all young animals that were still actively growing?), so there's a possibility at least some of that liver Vitamin A was redistributed to adipose and/or muscle tissue.

There is at least one publication that indicates Vitamin A is used in carbohydrate metabolism. That might somehow explain the results from these diabetic mice, and why people like Paul Saladino give up on a carnivore diet and go back to sugarland.

It's a shame they never seem to look for Vitamin A in other tissues in these studies, and seldom do they look at Vitamin A in the feces and urine. My big question is always, where did it actually go?! It seems like a stretch to assume it is always fully excreted from the body.

Something of note in the study Grant posted is that the authors attributed the final amount of Vitamin A in the liver directly to food consumption. However, the control group was reported to consume 68% and 74% of the food that diabetic and diabetic + insulin groups consumed, respectively (during the last 3 weeks of the study...we need to know what it was for the entire study to get a full comparison of Vitamin A intake though), whereas the final liver Vitamin A level in the the control group was 62% and 57% of diabetic and diabetic + insulin groups, respectively. That suggests a disproportionate accumulation of Vitamin A in the livers of insulin-treated rats who ate 36% more food than controls but had 76% more Vitamin A stored in their livers than controls.

On the other hand, in a study cited within the one Grant posted, diabetic rats treated with insulin had less Vitamin A stored in the liver than controls after a period of explicit Vitamin A supplementation. Not sure how to make sense of those apparently disparate results (different amounts or forms of insulin, or different affects of the toxin that was used to make the animals "diabetic"?).

Of interest in this latter study, all animals that were supplemented with Vitamin A and which subsequently underwent a Vitamin A "depletion" period appear to have lost a minimum of half their liver stores within only 12 days! Animals injected with insulin lost far more than controls. It's hard to believe all that Vitamin A was excreted from the body so quickly. For some reason, virtually all of the study groups gained weight during both the Vitamin A supplementation period and during the "depletion" period that followed (maybe because they were all young animals that were still actively growing?), so there's a possibility at least some of that liver Vitamin A was redistributed to adipose and/or muscle tissue.

There is at least one publication that indicates Vitamin A is used in carbohydrate metabolism. That might somehow explain the results from these diabetic mice, and why people like Paul Saladino give up on a carnivore diet and go back to sugarland.

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#7 · October 20, 2023, 1:27 pm

Anecdotally speaking, even Vitamin D supplements caused me to feel 'dry'. I had a period of dry eyes lasting 3-4 months after taking some strong pharmaceuticals for another reason for about a month.

I think the core is this: adding anything to the body that might displace things in the liver causes excessive retinol to come out

#8 · October 30, 2023, 1:15 pm

Quote from David on October 30, 2023, 1:15 pm
@ggenereux2014

I have looked a little bit into insulin and I found that pharmaceutical preparations of injectable insulin usually contains zinc in some form and amount. I think zinc + insulin have been a thing since around 1933 to make insulin effective for a longer time:
"In 1923, the first commercial insulin product was produced. Though this insulin was life-saving, it was far from perfect. It was extracted from animal pancreata and thus was not human insulin, was difficult to purify and produce, was unstable, and did not last long in the body. Scientists continued to study insulin to develop solutions to these problems. For example, a decade later, they discovered that the addition of the molecules protamine and zinc produced a long-acting animal insulin that required fewer injections throughout the day."
https://www.niddk.nih.gov/news/archive/2021/celebrating-discovery-development-insulin

I also just searched up a 1998 study on zinc and diabetes, called:
"Zinc, insulin and diabetes"
https://pubmed.ncbi.nlm.nih.gov/9550453/

Here is the abstract from the 1998 study (I have bolded a part of it):
"The relationship between diabetes, insulin and zinc (Zn) is complex with no clear cause and effect relationships. In Type 1 diabetes there is a lack of insulin production, in Type 2 diabetes resistance to the effects of insulin are predominant. Both Type 1 and Type 2 have the same long-term complications. Diabetes effects zinc homeostasis in many ways, although it is most probably the hyperglycemia, rather than any primary lesion related to diabetes, which is responsible for the increased urinary loss and decreases in total body zinc. The role of Zn deficiency, which could, at least potentially, exacerbate the cytokine-induced damage in the autoimmune attack which destroys the islet cell in Type 1 diabetes, is unclear. Since Zn plays a clear role in the synthesis, storage and secretion of insulin as well as conformational integrity of insulin in the hexameric form, the decreased Zn, which affects the ability of the islet cell to produce and secrete insulin, might then compound the problem, particularly in Type 2 diabetes. Several of the complications of diabetes may be related to increased intracellular oxidants and free radicals associated with decreases in intracellular Zn and in Zn dependent antioxidant enzymes. There appears to be a complex interrelationship between Zn and both Type 1 and Type 2 diabetes. The role of Zn in the clinical management of diabetes, its complications, or in its prevention is, at best, unclear."

Here is an excerpt about one type of injectable insulins, NovoLog (there seems to be another version also called NovoLog Mix 70/30, "NovoLog Mix 70/30 is a product which contains 30% insulin aspart and 70% insulin aspart protamine."):
"Insulin Aspart injection is a sterile, clear, and colorless solution for subcutaneous or intravenous use. Each mL contains 100 units of insulin aspart and the inactive ingredients: disodium hydrogen phosphate dihydrate (1.25 mg), glycerin (16.0 mg), metacresol (1.72 mg), phenol (1.50 mg), sodium chloride (0.58 mg), zinc (19.6 mcg), and Water for Injection, USP. Insulin Aspart has a pH of 7.2-7.6. Hydrochloric acid 10% and/or sodium hydroxide 10% may be added to adjust pH."
https://www.drugs.com/pro/insulin-aspart-injection.html

@ggenereux2014

I have looked a little bit into insulin and I found that pharmaceutical preparations of injectable insulin usually contains zinc in some form and amount. I think zinc + insulin have been a thing since around 1933 to make insulin effective for a longer time:
"In 1923, the first commercial insulin product was produced. Though this insulin was life-saving, it was far from perfect. It was extracted from animal pancreata and thus was not human insulin, was difficult to purify and produce, was unstable, and did not last long in the body. Scientists continued to study insulin to develop solutions to these problems. For example, a decade later, they discovered that the addition of the molecules protamine and zinc produced a long-acting animal insulin that required fewer injections throughout the day."
https://www.niddk.nih.gov/news/archive/2021/celebrating-discovery-development-insulin

I also just searched up a 1998 study on zinc and diabetes, called:
"Zinc, insulin and diabetes"
https://pubmed.ncbi.nlm.nih.gov/9550453/

Here is the abstract from the 1998 study (I have bolded a part of it):
"The relationship between diabetes, insulin and zinc (Zn) is complex with no clear cause and effect relationships. In Type 1 diabetes there is a lack of insulin production, in Type 2 diabetes resistance to the effects of insulin are predominant. Both Type 1 and Type 2 have the same long-term complications. Diabetes effects zinc homeostasis in many ways, although it is most probably the hyperglycemia, rather than any primary lesion related to diabetes, which is responsible for the increased urinary loss and decreases in total body zinc. The role of Zn deficiency, which could, at least potentially, exacerbate the cytokine-induced damage in the autoimmune attack which destroys the islet cell in Type 1 diabetes, is unclear. Since Zn plays a clear role in the synthesis, storage and secretion of insulin as well as conformational integrity of insulin in the hexameric form, the decreased Zn, which affects the ability of the islet cell to produce and secrete insulin, might then compound the problem, particularly in Type 2 diabetes. Several of the complications of diabetes may be related to increased intracellular oxidants and free radicals associated with decreases in intracellular Zn and in Zn dependent antioxidant enzymes. There appears to be a complex interrelationship between Zn and both Type 1 and Type 2 diabetes. The role of Zn in the clinical management of diabetes, its complications, or in its prevention is, at best, unclear."

Here is an excerpt about one type of injectable insulins, NovoLog (there seems to be another version also called NovoLog Mix 70/30, "NovoLog Mix 70/30 is a product which contains 30% insulin aspart and 70% insulin aspart protamine."):
"Insulin Aspart injection is a sterile, clear, and colorless solution for subcutaneous or intravenous use. Each mL contains 100 units of insulin aspart and the inactive ingredients: disodium hydrogen phosphate dihydrate (1.25 mg), glycerin (16.0 mg), metacresol (1.72 mg), phenol (1.50 mg), sodium chloride (0.58 mg), zinc (19.6 mcg), and Water for Injection, USP. Insulin Aspart has a pH of 7.2-7.6. Hydrochloric acid 10% and/or sodium hydroxide 10% may be added to adjust pH."
https://www.drugs.com/pro/insulin-aspart-injection.html

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Insulin stimulates the release of vitamin A stores from the liver (Bowles, 1967)

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