I've read fish oil lowers triglycerides

Jennifer72 · 2019-12-18 02:35:07 UTC

… but the books I’ve read don’t say how. I know that triglycerides are manufactured by the liver via lipogenesis to convert excess glucose to fat.

Is it because the omega 3 in fish oil puts the omega 6 : omega 3 ratio more in balance causing less inflammation? Less inflammation means less stress on the body, which results in less cortisol, less blood glucose, less insulin and then ultimately less trigs?

If that’s the case then the fish oil not only helps with triglycerides but with the metabolic syndrome in general. Getting those in balance should really improve my blood glucose control over time and help with weight loss right?

I have so much omega 6 stored, I have to keep that in mind… most of my energy for the day is coming from omega 6 rich adipose tissue right now. So I guess this means I should consume plenty of omega 3 fish / fish oil right? Been getting 1490 EPA and 1000 DHA per day. (1 tsp twice per day of Nordic Naturals Omega 3 triglyceride oil.). Should I consume more than that since I am 362 lbs and burn a lot more than someone half my size?

PaulL · 2019-12-18 03:14:56 UTC

Not really, because ω-3 and ω-6 fatty acids, while essential to the diet, are needed only in a small quantity. And too much of the ω-6 fatty acids causes systemic inflammation. It’s the quantity involved, not the ratio.

The way to improve your blood glucose control is to stop consuming glucose—which is what all carbohydrates are, long chains of glucose molecules. If you were to eliminate carbohydrate completely from your diet, you would find that your liver would make a very small quantity of glucose, just enough to feed your red blood cells and the other cells throughout your body that are incapable of metabolising fatty acids. If you eat more than that quantity of glucose, the extra gets converted into fatty acids, combined into triglycerides, and stored in your fat tissue.

The ω-3 and ω-6 fatty acids are types of polyunsaturated fatty acid. The challenge with the standard American diet is not only to get enough ω-3 and ω-6 in the right balance, but also to avoid getting too much ω-6. This is why you should be cooking with butter/ghee, tallow, lard, or bacon fat, and using seed oils (avocado, coconut, and olive), which have a much more reasonable ω-6 content. Some of the so-called “vegetable” oils on the market (they are actually seed oils, which is the term the industry uses internally) contain a phenomenally high percentage of ω-6 fatty acids—so much as to be actively detrimental to our health.

If you stick to fat sources that provide primarily saturated and monounsaturated fat, you should notice a drop in your triglycerides and an increase in your HDL cholesterol. A ratio of triglycerides to HDL of 2.0 or less (0.9 or less in the measurements common outside of North America) is a guarantee of low cardiovascular risk. This improvement in your lipid numbers will result from the saturated fat; whereas the monounsaturated fat is what your muscles will primarily metabolise for their energy. As long as you keep your carbohydrate intake low enough, you body will be able to use both the fat in your food and the excess stored fat in your fat tissue (and especially any visceral fat you may have accumulated, it is the first to go). But the caveat there is that you can’t skimp on the calories, or you body will go into famine mode and try to hang on to its fat stores. The trick is to eat enough to keep your metabolic rate high, so your body will feel free to shed the excess stored fat.

Jennifer72 · 2019-12-18 14:28:37 UTC

I just want to know why fish oil alone lowers triglycerides. Dr. William Davis says it does and studies show it does. How?

Is it because the person is now getting the necessary omega 3 and it results in less inflammation which means less stress, less cortisol, less insulin and less lipogenesis. Omega 3 fish oil alone is supposed to lower triglycerides independent of the amount of omega 6 you ingest.

I know if you keep omega 6 oils down along with glucose, it will improve inflammation. And I incorporate that into my diet. I eat no vegetable oils nor processed food, limit PUFA fat and I eat 15g net carbs per day along with moderated protein at 60-70g per day.

I just want to know why adding omega 3 fish oil to ANY diet improves trigs. Studies have shown that it does, without regard to diet.

Jennifer72 · 2019-12-18 14:45:29 UTC

So I’ve updated my little metabolic syndrome flowchart… Added in omega 6 and omega 3… The circled blue part below in the chart… does that look right? i.e. too much omega 6 and/or too little omega 3. So a lack of omega 3 alone causes inflammation, regardless of omega 6 correct? Say you keep omega 6 way down but don’t have enough omega 3… still results in inflammation.

ctviggen · 2019-12-18 20:48:56 UTC

Just saw some recent studies indicating O3 is better absorbed in conjunction with saturated fat.

amwassil · 2019-12-18 21:12:13 UTC

This is wrong. Gluconeogenesis is demand driven not supply driven. In the absence of dietary glucose, gluconeogeneis creates only enough glucose to supply those cells and organs that cannot utilize fatty acids and/or ketones for energy. That is a fairly low amount overall. Just because you eat more protein than you need for immediate maintenance and repair, it does not convert to glucose. Most will get used for energy, albeit much less efficiently than fats/ketones. In addition, gluconeogenesis can use fatty acids as its raw ingredient just as well as amino acids.
jenn72

Jennifer72 · 2019-12-18 22:12:48 UTC

I can quote at least 10 very popular keto / fasting books that say excess protein converts to glucose. It certainly is in my case… and I imagine in most others as well. I realize there is bioindividuality. Perhaps you aren’t that insulin resistant (if that has something to do with it) I don’t know… I imagine most people on this forum are.

FYI, Besides protein and fat, gluconeogenesis also utilizes lactic acid.

You mentioned this before on another thread. ANyways this thread is about fish oil. I am trying to understand how omega 3 alone can reduce trigs.

Justin_Jordan · 2019-12-18 22:09:35 UTC

There’s also the assumption that because GNG is demand driven, that the demand signalling works properly which, uh, is a dubious proposition.

It’s absolutely certain that in type one diabetics, if you keep carbs and fat stable, then varying degrees of protein consumption will usually require more insulin to keep blood sugar levels stable. On average, 1.5 times as much, but the number actually varies from somewhat less insulin to 9 times the original dose.

So, you know, the relationship between protein and blood glucose isn’t anywhere near as a straightforward as people would apparently like it to be.

Jennifer72 · 2019-12-18 22:45:11 UTC

All I know is it raises my blood glucose and I’ve shared this diagram with many on another forum who are also type 2 diabetic and eat keto, and none of them complained about it. It’s only on this forum to I get a couple who tell me I am wrong, and all the authors are wrong. All my type 2 diabetic friends experience this as well.

Jennifer72 · 2019-12-18 22:17:13 UTC

Anyways, I’d like for this thread to remain on topic please… I don’t care to talk about gluconeogenesis in this thread… It’s unrelated to fish oil.

ctviggen · 2019-12-18 23:46:12 UTC

There’s likely something wrong with your glucagon. Listen to the latest Diet Doctor podcast with Ben Bikman.

I can eat MASSIVE amounts of protein and get zero blood sugar rise - ever. It’s because I have a normal glucagon response. I’m not type 2 though.

Jennifer72 · 2019-12-19 00:53:18 UTC

Then I guess there must be something wrong with virtually everyone’s glucagon, since Phinney, Hallburg, Westman, Jason Fung, Jimmy Moore, etc… say to moderate protein because excess is converted to glucose.

And just because you don’t get a blood glucose rise doesn’t mean you aren’t generating massive amounts of insulin to cover the excess protein. All it could mean is you have a very robust pancreas. Also have you had your insulin resistance checked? HOMA-IR… $35 blood test from LifeExtension.com (fasting insulin + fasting glucose … 14 hour water only fast). My HOMA-IR is 3.61, very insulin resistant.

Do you have any weight to lose? If so are you losing it eating as much protein as you say? If so, then I guess you are not very insulin resistant?

amwassil · 2019-12-19 03:14:26 UTC

Here’s what Phinney says (nothing about gluconeogenesis):

On the other hand, too much dietary protein can drive down ketones for several reasons. Protein has a moderate insulin stimulating effect; and though less than the impact of a similar amount of carbohydrate consumption, high protein intakes can drive down ketone production in the liver (Marliss 1978). In fact, specific amino acids like alanine are potently anti-ketogenic. Additionally, when consumed to excess, protein can upset gastro-intestinal function and place a stress on the kidneys to remove the additional nitrogen.

For the most part, ‘excess’ protein, whatever that means for you, just becomes expensive calories.

amwassil · 2019-12-19 05:04:49 UTC

Finally, from:
Diabetes Spectrum
Volume 13 Number 3, 2000, Page 132

In Brief
People with diabetes are frequently given advice about protein that has no scientific basis…

Does 50–60% of protein become glucose and enter the bloodstream in 3–4 hours?

…

This raises the question of why, if gluconeogenesis from protein occurs, does the glucose produced not appear in the general circulation? Several theories have been suggested. The first is that considerably less than the theoretical amount of glucose (50–60%) produced from protein actually is produced and enters the general circulation, and the small amount of glucose released is matched by a corresponding increase in glucose use, if adequate insulin is available.⁴ Another theory suggests that the process of gluconeogenesis from protein occurs during a 24-hour period, and the slowly and evenly produced glucose can be disposed of over a long period of time.⁵ It is also speculated that the insulin stimulated by dietary protein causes the glucose formed to be rapidly stored as glycogen in the liver and in skeletal muscles. This glucose can then be released when insulin levels are low or glucagon levels are elevated, and the body does not identify if the glucose is from protein or carbohydrate.

To understand this process of gluconeogenesis and the question of why protein does not affect blood glucose levels, it is helpful to briefly review the metabolism of dietary proteins. The majority of protein is digested, and the amino acids not used for gut fuel are metabolized in the intestinal mucosal cells and transported by the portal vein to the liver for protein synthesis or gluconeogenesis.¹² In the liver, nonessential amino acids are largely deaminated, and the amino group (nitrogen) removed is converted into urea for excretion in the urine.¹³ It has been shown that in subjects without and with mild type 2 diabetes, ~50–70% of a 50-g protein meal is accounted for over an 8-hour period by deamination in the liver and intestine and synthesis to urea.¹⁴ It has been assumed that the remaining carbon skeletons from the nonessential amino acids are available for glucose synthesis, which would then enter into the general circulation.

The essential amino acids pass through the liver into the general circulation, where they may be removed and used for new protein synthesis or, alternatively, for skeletal muscle fuel. Circulating amino acids stimulate insulin and glucagon secretion. The amino acids that stimulate glucagon are different from those that stimulate insulin secretion.^15-17

To add to the confusion, the effect of protein on glucose appearance is influenced by insulin availability. With insulin deficiency, the oxidation of branched chain amino acids in muscle and uptake of alanine (the principle glycogenic amino acid) by the liver is accelerated, resulting in increased gluconeogenesis and augmented protein catabolism.¹⁸ The accompanying rise in glucose levels is most likely due to an increased conversion of ingested protein into glucose and to a decreased glucose removal rate. In subjects with diabetes who had insulin withheld for 24 hours, there was a three- to fourfold increase in liver glucose output after protein ingestion.¹⁹ However, in the presence of insulin, alanine uptake by the liver is virtually zero,²⁰ and hepatic glucose production falls by 85%.²¹ Indirectly then, insulin could reduce gluconeogenesis in the liver by decreasing the amino acid substrate supply. Insulin also inhibits the degradation of body proteins and lowers the circulating concentration of many amino acids.²²

The net effect on glucose output by the liver depends on the ratio of insulin to glucagon. In people with type 1 or type 2 diabetes, the glucagon response to protein is considerably greater than in people without diabetes.⁴ Glucagon stimulates an increase in hepatic glucose production due to an increase in glycogenolysis and an increase in gluconeogenesis. Glucagon antagonizes the effect of insulin in the liver. However, it does not antagonize the insulin-stimulated uptake of glucose in muscle or the insulin-mediated decrease in release of non-esterified fatty acids from fat cells.⁴

Therefore, the process of gluconeogenesis is affected by substrate supply and level of glycemic control. However, in people with well-controlled diabetes, minimal amounts of hepatic glucose are released into the general circulation after the ingestion of protein.

...

References

4 Gannon MC, Nuttall FQ: Protein and diabetes. In: American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Franz MJ, Bantle JP, Eds. American Diabetes Association, Alexandria, Va., 1999, p. 107-25.

5 Conn JW, Newburgh LH: The glycemic response to isoglucogenic quantities of protein and carbohydrate. J Clin Inves t 15:667-71, 1936.

6 Nuttall FQ, Gannon MC: Plasma glucose and insulin response to macronutrients in nondiabetics and NIDDM subjects. Diabetes Care 14:824-38, 1991.

7 Westphal SA, Gannon MC, Nuttall FQ: The metabolic response to glucose ingested with various amounts of protein. Am J Clin Nutr 52:267-72, 1990.

8 Khan MA, Gannon MC, Nuttall FQ: Glucose appearance rate following protein ingestion in normal subjects. J Am Coll Nutr 11:701-706, 1992.

9 Krezowski PA, Nuttall FQ, Gannon MC, Bartosh NH: The effect of protein ingestion on the metabolic response to oral glucose in normal individuals. Am J Clin Nutr 44:847-56, 1986.

10 Nuttall FQ, Mooradian AD, Gannon MC, Billington CJ, Krezowski PA: Effect of protein ingestion on the glucose and insulin response to a standardized oral glucose load. Diabetes Care 7:465-70, 1984.

11 Gannon MC, Damberg G, Gupta V, Nuttall FQ: Ingested protein has little effect on glucose concentration or rate of glucose appearance in people with type 2 diabetes [Abstract]. J Am Coll Nutr 18:546 (Abstract no. 97), 1999.

12 Nuttall FQ, Gannon MC: Plasma glucose and insulin response to macronutrients in nondiabetics and NIDDM subjects. Diabetes Care 14:824-38, 1991.

13 Windmueller HG, Spaeth AE: Uptake and metabolism of plasma glutamine by the small intestine. J Biol Chem 249:5070-79, 1978.

14 Nuttall FQ, Gannon MC: Metabolic response to dietary protein in people with and without diabetes. Diab Nutr Metab 4:71-88, 1991.

15 Floyd JC, Fajans SS, Conn JW, Knopf RF, Rull J: Insulin secretion in response to protein ingestion. J Clin Invest 45:1479-86, 1966.

16 Rabinowitz D, Merimee TJ, Maffezzoli R, Burgess JA: Patterns of hormonal release after glucose, protein, and glucose plus protein. Lancet ii :454-57, 1966.

17 Muller WA, Faloona FR, Aquilar-Parada F, Unger RH: Abnormal alpha-cell function in diabetes: response to carbohydrate and protein ingestion. N Engl J Med 28:109-15, 1970.</p<

18 Felig P, Wahren J, Sherwin R, Palaiologos G: Amino acid and protein metabolism in diabetes mellitus. Arch Intern Med 137:507-13, 1977.

19 Wahren J, Felig P, Hagenfeldt L: Effect of protein ingestion on splanchnic and leg metabolism in normal man and in patients with diabetes. J Clin Invest 57:987-99, 1976.
20 Felig P, Wahren J, Hendler R: Influence of oral glucose ingestion on splanchnic glucose and gluconeogenic substrate metabolism in man. Diabetes 24:468-75, 1975.
21 Felig P, Wahren J: Influence of endogenous insulin secretion on splanchnic glucose and amino acid metabolism in man. J Clin Invest 50:1702-11, 1971.

22 Zinnerman HH, Nuttall FQ, Goetz FG: Effect of endogenous insulin on human amino acid metabolism. Diabetes 15:5-8, 1966.

23 Wolever TMS, Nguyen P-M, Chiasson J-L: Determinants of the diet glycemic index calculated retrospectively from diet records of 342 individuals with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 59:1265-69, 1994.

24 Nordt TK, Besenthal I, Eggstein M, Jakober B: Influence of breakfasts with different nutrient contents on glucose, C peptide, insulin, glucagon, triglycerides, and GIP in non-insulin-dependent diabetics. Am J Clin Nutr 53:155-60, 1991.

Justin_Jordan · 2019-12-19 05:58:37 UTC

I.e. it’s demand driven except when it isn’t.

Fruno · 2019-12-19 08:23:33 UTC

We have so many things that we overturn once we start to question it. Until 5 years ago or whatever a LOT of people that I respect very much would say “fibre is good, fibre is necessary”. Then some people like Paul Mason looked closer and realized that the science says otherwise.

The insulin response of meat might be one of these issues. I always thought meat causes an insulin spike and is converted to glucose until I watched Ben Bikmans talk. I wonder if all the people you named would still say the same about meat.

We know for a fact that people on carnivore diet often have very low triglyceride values, which would indicate that only very little meat is converted to glucose.

Fruno · 2019-12-19 08:33:51 UTC

That’s probably a great example of why we believe in flawed science (I haven’t read the referenced study though.) Meat causes an insulin spike for people on a western diet but not on keto. I’d bet that all people studied there were on a western diet, hence the result was “yes, meat does indeed cause insulin spikes”. Case closed, never looked at again. Except that it is wrong of course

Personally I think that we need to start over with nutritional science. Build a new set of studies that have been looked at carefully. For any dietary intervention we’ll need to differentiate at least 4 groups: High carb insulin sensitive, high carb insulin resistant, low carb insulin sensitive, low carb insulin resistant. Results can differ a LOT, for example we know that people CAN lose weight efficiently with calorie restriction on a high carb diet if (and only if) they are insulin sensitive.

I certainly know that my ketone levels are higher since I went (almost) carnivore. n=1, moderately insulin resistant (one year of low carb), keto diet.

daddyoh · 2019-12-19 08:56:41 UTC

Very N=1 but yesterday I had 8 oz of ground beef and 4 oz of stewed pork for lunch. 30 min after my BG was 83 mg/dL and I’m sure I’m still slightly insulin resistant.

FYI - My fasted BG can still be over 100 in the early morning hours. The so called dawn affect.

Fangs · 2019-12-19 13:16:06 UTC

does this help?

Jennifer72 · 2019-12-19 15:32:49 UTC

daddyoh, it takes 8 hours for protein to be processed by the body unlike carbs which is 30 mins to 2 hours on average. I never get a spike in blood glucose eating excess protein until hours and hours later, like when I wake up with fasting blood glucose over 110 instead of 75 mg/dL.