164 replies to this topic

[pamojja]

 After this post I was under the impression you had a recent insulin tested?

 

Thanks guys. I did a recent insulin test with glucose and it was in the normal range.

 

 

[Mind]

Right now I am doing intermittent fasting. Monday through Friday I do about 20 hour fast, then 4 hours of eating. It is easier to do when I am busy at work. I stop eating about 4 hours before going to sleep. Then I sleep for 6-8 hours, then I go to work for 7-9, then I come home and eat. It is easier to fast when I keep busy at work. Keeping the mind active and not thinking about food is the key for me.

Edited by Mind, 15 November 2021 - 03:48 PM.

[Nate-2004]

After this post I was under the impression you had a recent insulin tested?

Yes a glucose tolerance test is what I did.

[pamojja]

I did a recent insulin test with glucose and it was in the normal range.

 

Yes a glucose tolerance test is what I did.

 

An fasting insulin is different from what is tested with the glucose tolerance test. Where after a bolus of glucose intake, the blood-glucose response in different time-intervals is tested. An insulin test tests for blood insulin, a glucose tolerance test for blood glucose.

 

[Nate-2004]

An fasting insulin is different from what is tested with the glucose tolerance test. Where after a bolus of glucose intake, the blood-glucose response in different time-intervals is tested. An insulin test tests for blood insulin, a glucose tolerance test for blood glucose.

Ok thanks I guess I’ll have to see a doctor for an insulin test

[Nate-2004]

So here's another possible reason why my A1C is so high:

 

The FTO gene, the major genetic risk factor for obesity, codes for the fat mass and obesity associated protein. There is a cluster of polymorphisms in the FTO gene that increase obesity risk. This genotype, rs17817449(G;G), has been associated with a 1.7-fold increased obesity risk and saturated fat may have a negative effect on blood glucose and insulin levels. There are common polymorphisms in the FTO gene, which codes for the fat mass and obesity associated protein. The rs17817449 polymorphism is located in the intronic region of theFTO gene. This particular polymorphism is . in individuals with the (G;G) genotype. Other gene polymorphisms in the , particularly in the context of a . Saturated fat is found in fatty beef, pork, coconut oil, butter, cheese, and other dairy products, while polyunsaturated fats are found in foods like nuts and fatty fish such as salmon and herring. This research suggests that individuals at high risk of obesity due to FTO polymorphisms, such as this one, may benefit from having a higher polyunsaturated fat intake and a lower saturated fat intake. SNPs Involved rs17817449(G;G)

 

The FTO gene, the major genetic risk factor for obesity, codes for the fat mass and obesity associated protein. Ghrelin, often called the hunger hormone, is produced when the stomach is empty and is thought to stimulate appetite and desire to eat. This genotype, rs9939609(A;A), has been associated with an increased risk of obesity and type 2 diabetes due to high production of ghrelin. There are common polymorphisms in the FTO gene, which codes for the fat mass and obesity associated protein. The rs9939609 polymorphism is located in the intronic region of theFTO gene. This particular polymorphism is . The A allele is associated with higher levels of the appetite-stimulating hormone ghrelin, as well as a roughly 60% increased risk of obesity and type 2 diabetes. Higher ghrelin levels are associated with over-eating due to lack of satiation. Macronutrient composition of the first meal of the day has been shown to affect ghrelin levels. compared to those who ate an isocaloric diet that was low in carbohydrates. These results suggest that a breakfast high in carbohydrates and protein may help reduce ghrelin levels and facilitate greater satiety. Sleep has also been shown to be an important regulator of ghrelin levels. This suggests that adequate sleep may be an important factor in maintaining normal ghrelin levels. The (A;A) genotype has particularly in the context of a . Saturated fat is found in fatty beef, pork, coconut oil, butter, cheese, and other dairy products, while polyunsaturated fats are found in foods like nuts and fatty fish such as salmon and herring. This research suggests that individuals that are at high risk of obesity due to FTO polymorphisms, such as this one, may benefit by having a higher polyunsaturated fat intake and a lower saturated fat intake. SNPs Involved rs9939609(A;A)

 

The FTO gene, the major genetic risk factor for obesity, codes for the fat mass and obesity associated protein. There is a cluster of polymorphisms in the FTO gene that increase obesity risk. This genotype, rs1121980(T;T), has been associated with a 2.76-fold increased risk of obesity particularly with saturated fat. There are common polymorphisms in the FTO gene, which codes for the fat mass and obesity associated protein. The rs1121980 polymorphism is located in the intronic region of theFTO gene. This particular polymorphism is . The (T;T) genotype has particularly in the context of a . Saturated fat is found in fatty beef, pork, coconut oil, butter, cheese, and other dairy products, while polyunsaturated fats are found in foods like nuts and fatty fish such as salmon and herring. This research suggests that individuals at high risk of obesity due to FTO polymorphisms, such as this one, may benefit from having a higher polyunsaturated fat intake and a lower saturated fat intake. is associated with lower circulating levels of 25-OHD raises serum 25-hydroxy vitamin D levels by 5-10 ng/ml. According to the endocrine society Meta-analyses have shown that people with serum levels between 40-60 ng/ml have the lowest all-cause mortality. Read more on SNPedia. Read more about other SNPs that are associated with a higher all-cause mortality. Read more about genetic risk for vitamin D deficiency and multiple sclerosis. one of many in this gene that influence genetic obesity risk Obese individuals who ate a meal high in fiber-rich carbohydrates and protein had significantly lower postprandial ghrelin levels Sleep loss has been shown to significantly increase ghrelin levels in healthy, normal weight individuals. also been associated with obesity high saturated fat and low polyunsaturated fat intake Read more about rs9939609 on SNPedia one of many in this gene that influence genetic obesity risk been associated with a 2.76-fold increased risk for obesity high saturated fat and low polyunsaturated fat intake SNPs Involved rs1121980(T;T)

 

Back when I started doing keto and fasting, I increased my fat intake pretty dramatically overall, especially during keto. I've no doubt that saturated fat was pretty high. I also use coconut cream in my coffee, which probably doesn't help matters. 

 

I think what I might do, while I still plan to satisfy my sweet tooth with stevia and erythritol substitutes, I'm going to greatly cut down on saturated fat everywhere I can. I'll switch to just almond milk in my coffee instead of the tasty combo I've been using. I will somehow avoid pizza and cheese, I don't know how because cheese is enjoyment of life IMO. All the foods I love and enjoy are all foods that are killing me I guess. Naturally. Longevity and youth is torture.

 

 

[pamojja]

So here's another possible reason why my A1C is so high:

 

The most likely reason is that the life-cycle of your HbA1c got longer by lower carb intake, and thereby more glycation acumulating in haemoglobin. Also I wouldn't be overly concerned in your case. BG meassurement isn't as easily falsified. And a 110 mg/dl after dessert is actually still an excellent blood sugar control.
 

Edited by pamojja, 23 November 2019 - 01:29 PM.

[Nate-2004]

The most likely reason is that the life-cycle of your HbA1c got longer by lower carb intake, and thereby more glycation acumulating in haemoglobin. Also I wouldn't be overly concerned in your case. BG meassurement isn't as easily falsified. And a 110 mg/dl after dessert is actually still an excellent blood sugar control.
 

 

I wish I could say I was consistent with the lower carb intake but I wasn't. I was good when I did keto and when I was alternate day fasting but something had to give during those times. I think I just made things worse. You're right that 110 after a dessert is good, but that was with metformin. I think I'm going to try 3 months of lowering my sat fat and see if things change, but continue with the 16 hour daily fasts between 6 and 10 am. There's gotta be some way of switching up recipes, finding cheese alternatives and changing to just almond milk without the coconut without being miserable.

[Nate-2004]

I solved my fasted blood glucose and blood pressure in one fell swoop of keeping saturated fat below 13g. That's literally the only change I made two weeks ago. I'm at 84 in the morning now instead of 120. My systolic dropped by 15 pts back to normal. My skin even looks better. I really regret not taking that advice from 23 and Me more seriously nearly 4 years ago when this all started, but I was skeptical of it at first. Now I know that diet should be highly tailored to one's genetics and that really only makes sense when considering all the studies done on fad diets and their inconsistent results.

 

I still don't eat anything after 6pm and really, if I got home from work before 5pm I'd wouldn't eat after 5 but it's hard to manage that with my schedule. So I go about 16 hrs without food each day.

 

The down side to this is that I have to eat fish like a bear. Salmon in particular. Which may get old soon. 

Edited by Nate-2004, 14 December 2019 - 08:42 PM.

[ambivalent]

Worth remembering some fluctuations in HbA1c might occur due to ribose if you've been taking it:

 

https://www.scienced...352396417303936

[Amira L.]

I found eating low carb for a few days helped me acclimate. From there, I stopped eating anything before noon and after 8pm. This is 16/8. I did it for a few weeks (it was a big rough, you'll get hungry). But this goes away quickly if you stick with it. Soon the hunger goes away permanently.  If you're seeing good results, you can stick with the 16/8. 

[jroseland]

I've been fasting for years, in fact, it's a major economic lifehack, so I decided to read Dave Asprey's recent deep-dive book on the topic, Fast This Way. The book is a bit of a memoir actually, it's punctuated by vignettes from a grueling (and transformative) 4-day fast that the author did alone in a cave in the Arizona desert.

The book gets 5-stars from me. It captures the state-of-the-art science on the ancient practice of fasting, is packed with pragmatic takeaways, and the story-telling is compelling. I put it down wondering where I could do a 4-day spiritual fast in a cave, like Dave!

 

 

Listen to podcast: The EDIFYING economic biohack (that you may not be getting right...) Fast This Way [⭐⭐⭐⭐⭐ Book Review]

[Mind]

I found eating low carb for a few days helped me acclimate. From there, I stopped eating anything before noon and after 8pm. This is 16/8. I did it for a few weeks (it was a big rough, you'll get hungry). But this goes away quickly if you stick with it. Soon the hunger goes away permanently.  If you're seeing good results, you can stick with the 16/8. 

 

I was surprised by how my hunger pains became very manageable. I just don't notice them very much. Then I again, I do stay busy during the work-day/fasting period, so I don't give my mind to much time to dwell upon it. If I was just sitting around the house watching TV or something, I suspect I would think about food a lot more often.

[Danniel]

I discovered that it's surprisingly easy for me to fast for about 60 hours. Every week I fast Monday, Tuesday a good part of Wednesday. Are there any dangers or side effects for doing this?

How can I get maximum out of it? Advice about things to take/do before/during/after for stem cells renewal, mitochondrial health, clearing senescent cells?

 

[sensei]

I just finished a 60 hour fast. It was easier than I expected, but, I have been performing a walk -up series of one 36HR and 2 48HR fasts over the last two-three weeks.

Regarding some previous posts and blood sugar.

Long term ketotic diet can cause beneficial pseudo-diabetes. Ketosis causes body cells to become insulin resistant so all available glucose can be used by the brain.