Carbs, Not Saturated Fats, Increase Fat in Blood

Interesting study that gradually increased carbs and decreased fats shows that fats don’t increase fat in the blood, but carbs do (Volk BM, Kunces LJ, Freidenreich DJ, Kupchak BR, Saenz C, et al. (2014) Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLOS ONE 9(11): e113605.).

Sixteen adults with metabolic syndrome (age 44.9±9.9 yr, BMI 37.9±6.3 kg/m2) were fed six 3-wk diets that progressively increased carbohydrate (from 47 to 346 g/day) with concomitant decreases in total and saturated fat. Despite a distinct increase in saturated fat intake from baseline to the low-carbohydrate diet (46 to 84 g/day), and then a gradual decrease in saturated fat to 32 g/day at the highest carbohydrate phase, there were no significant changes in the proportion of total SFA in any plasma lipid fractions. Whereas plasma saturated fat remained relatively stable, the proportion of palmitoleic acid in plasma triglyceride and cholesteryl ester was significantly and uniformly reduced as carbohydrate intake decreased, and then gradually increased as dietary carbohydrate was re-introduced.

One of the Good Guys – Dr. Benjamin Bikman

I’ve spent too much time covering the keto hucksters (OK, mostly just Jimmy Moore but he’s a big enough target) so I thought I’d switch it up and look at one of the good guys – Dr. Benjamin Bikman (our YouTube playlist of Dr Bikman). I mentioned Ben in (Great BLOGs). He is a PhD who teaches at BYU and he’s got a lot to say about Protein over at his InsulinIQ site.

Here’s a video (High Intensity Health Episode 200) where he is interviewed.

Ben is one of the folks who came to nutrition from the exercise side. Ben really gets it about Insulin and obesity.

A video on Insulin and Glucagon.

 

Vegan Diet Blood Test Results

No, don’t worry. I have not gone vegan.  I took a look at another FASTER study participant (Damian Stoy) over on the Low Carb Studies Athletics BLOG (FASTER Subject 43). Damian is a vegetarian (or maybe vegan I can’t tell the difference). One of the results that Damian posted was his blood tests. They are generally pretty good but there’s one number that stood out.

Damian’s platelet count is below the reference range. What causes this? Turns out there is a study of this (Obeid R1, Geisel J, Schorr H, Hübner U, Herrmann W. The impact of vegetarianism on some haematological parameters. Eur J Haematol. 2002 Nov-Dec;69(5-6):275-9.).

CONCLUSION: vitamin B12 and iron status were compromised by a vegetarian diet. Variations in mean corpuscular volume were determined by iron and vitamin B12 status. Lower lymphocyte and platelet count were accompanied by metabolic evidence that indicated vitamin B12 deficiency.

Another study (Fisher M, Levine PH, Weiner B, Ockene IS, Johnson B, Johnson MH, Natale AM, Vaudreuil CH, Hoogasian J. The effect of vegetarian diets on plasma lipid and platelet levels. Arch Intern Med. 1986 Jun;146(6):1193-7.).

…platelets, which may also play a role, have also been observed to have aberrant functions in vegetarians.

This post has some suggestions for vegans to raise their platelet levels (Golden Vegetarian Eatery).

Or just eat some meat. Folic Acid.

 

Lowering Fasting Insulin

If the Insulin Theory of Obesity is correct then my question for Richard Morris, Jimmy Moore, and other obese Low Carb luminaries is:

@richard I am curious about your podcast intro. You say that all signs of disease are gone but I’ve also heard you state that your Fasting Insulin is high. That would suggest that at least one of the markers of Insulin Resistance is still present. Is that a concern for you and what are you doing to try and reverse that? Would further weight loss help? (I know you and Carl both say weight loss isn’t necessarily your goal). I know you ride your bike quite a bit so that sort of intervention seems only so helpful in your case.

Two of the signs of metabolic syndrome are waist circumference and fasting insulin levels. Richard and Jimmy have both stated they have high fasting insulin levels and they both have substantial waist circumferences.

My contention is that weight loss is necessary in order to lower fasting insulin. And yes, it is true that higher fasting insulin levels make it much harder to lose weight. Note I did not say impossible, just much harder. But they also make it much more important to lose weight.

Here’s evidence that fasting Insulin correlates to BMI. A great place for an answer to this question to look is very young people. There was an interesting study which looked at seven year old children (Hrafnkelsson H1, Magnusson KT, Sigurdsson EL, Johannsson E. Association of BMI and fasting insulin with cardiovascular disease risk factors in seven-year-old Icelandic children. Scand J Prim Health Care. 2009;27(3):186-91.). Here’s what they learned in these young children:

Some 14% of the participating children were classified as overweight. Overweight children had higher fasting insulin, higher fasting glucose, and higher systolic and diastolic blood pressure. Furthermore, they had significantly lower total cholesterol (TC), lower high-density lipoprotein (HDL), and lower low-density lipoprotein (LDL) but a similar TC/LDL ratio to normal-weight children. The factors that were strongly associated with BMI were serum fasting insulin, systolic blood pressure (SBP), HDL and fasting glucose, while the sum of four skinfolds, triglycerides, glucose, and LDL were highly associated with fasting insulin.

The LDL part is interesting (but not the subject of this thread).

BMI and fasting insulin are clearly correlated. Does one cause the other? Probably.  Does it actually matter? If lazy ket0 isn’t working then look around. Protein Sparing Modified Fasts are a special case of keto with low fat and low carbs. But the high fat kings won’t try them (recent pictures of Left to Right Richard Morris, Carl Franklin, and Jimmy Moore). As far as I know none of these guys will post their food diaries. In fact, they seem to not track their food intake.

  

Again, this is not intended to ridicule any of these men. Rather, it is to question their dietary advice. They are all low protein and high fat advocates. And it worked for them. Until it didn’t work.

 

Jimmy’s Big Fat Experiment

Jimmy Moore has been covered here a couple of times (Fat Jimmy and Jimmy Does PSMF – Sorta).

Jimmy’s Current Drama/Experiment

Now Jimmy is going to do an experiment to show the effect of eating 90% of his calories from fat. This is designed to contrast with Jimmy’s “failed” protein experiment. Remember that? It was the experiment which dropped Jimmy’s fasting Insulin in half but Jimmy considered it a failure.

Jimmy is going to eat 1900 calories for a week. Let me make a radical set of predictions (actually not radical at all).

  1. Jimmy will lose weight.
  2. Jimmy weighs north of 300 lbs so he must be taking in like 3500 calories a day.
  3. Dropping his calories to 1900 will create a deficit of around 1600 calories a day which should come from body fat.
  4. Jimmy should lose about 3-4 lbs of fat over the week.
  5. If Jimmy loses more 3-4 lbs that will be interesting since it will create a real mystery as to what he is eating prior to the diet since he would have to be at a large surplus prior to the experiment.
  6. Certainly Jimmy has enough fat on his body to support a long fast so this high fat diet will just supplement his body fat stores.
  7. Jimmy will proclaim fat the winner over protein.
  8. Jimmy is doing 1900 calories with 190 calories from protein or 47.5 grams of protein a day.
  9. If Jimmy currently weighs 300 lbs, that’s 136 kg. Jimmy will be taking in 0.35 g per kg of body weight.
  10. The DRI (Dietary Reference Intake) is 0.8 grams of protein per kilogram of body weight so Jimmy will be under half the DRI for protein.
  11. Jimmy’s cholesterol will go up since he’s going hypocaloric (See Dave Feldman).

Jimmy’s diet will be fat bombs.

Jimmy’s High Protein Experiment

What was Jimmy’s so-called High Protein diet? 1900 calories with 90% from protein is 1710 calories from protein or 427.5 grams of protein. That’s an extreme amount of protein. If Jimmy bothered to look at Ted Naiman’s graphic he would have seen:

TedTed Naiman’s graphic shows the ratio of protein to non-protein energy in grams. To maintain eat as many grams of fat as protein. To lose eat more protein and less fat. To gain weight eat less protein and more fat. Jimmy has been in that diet as he has gotten fatter.

Jimmy would do better to listen to Arnold.

LDL Increases During Massive Weight Losses

Very Low Calorie diets can cause LDL numbers to increase temporarily (Am J Clin Nutr. 1991 Jun;53(6):1404-10. The transient hypercholesterolemia of major weight loss. Phinney SD, Tang AB, Waggoner CR, Tezanos-Pinto RG, Davis PA.).

Abstract

Serum lipoproteins, body composition, and adipose cholesterol contents of six obese women were studied during and after major weight loss by very-low-calorie diets (VLCDs). Subjects started at 168 +/- 11% of ideal body weight, lost 30.3 +/- 3.7 kg in 5-7 mo, followed by 2+ mo in weight maintenance. Serum cholesterol fell from a prediet (baseline) value of 5.49 +/- 0.32 to 3.62 +/- 0.31 mmol/L (P less than 0.01) after 1-2 mo of VLCDs (nadir), after which it rose to 5.95 +/- 0.36 mmol/L (peak, P less than 0.01 compared with nadir and baseline) as weight loss continued. With weight maintenance, serum cholesterol fell to 4.92 +/- 0.34 mmol/L (P less than 0.05 compared with peak). Adipose cholesterol content did not change in peripheral (arm and leg) biopsy sites but rose significantly in abdominal adipose tissue with weight loss. We conclude that major weight loss was associated with a late rise in serum cholesterol, possibly from mobilization of adipose cholesterol stores, which resolved when weight loss ceased.

Here is a second paper on the same issue (Al Dahmani, Khaled Mohammed et al. Transient severe hypercholesterolemia following bariatric surgery treated successfully with increased food intake. Nutrition , Volume 32 , Issue 3 , 394 – 396).

…a case of transient severe hypercholesterolemia after bariatric surgery treated successfully with increased food intake. A 25-y-old policeman who had sleeve gastrectomy for morbid obesity 10 mo previously presented with generalized weakness, constipation, and significant weight loss after severe dietary restriction. All his preoperative and prior investigations were normal. Further investigation revealed severe total and low-density lipoprotein hypercholesterolemia. After all other causes of secondary hypercholesterolemia were excluded, a diagnosis of starvation-induced hypercholesterolemia was made. The patient was therefore started on a normal mixed diet gradually increased to achieve satiation. His dietary intake, body weight, and lipid profile were monitored over a 3-mo period. Eventually his symptoms abated, weight increased, and lipid profile returned back to normal levels. Although dietary management of failed weight loss after bariatric surgery is the main priority for health professionals, this case illustrates the possible harm of severe dietary restriction after surgery and the need for judicious dietary and nutritional management.

Hazard Ratios for LDL Particle Sizes

There are different types of LDL particles. They are classified by at least two phenotypes (A and B).

Phenotype B is associated with heart disease (LDL subclass phenotypes and triglyceride metabolism in non-insulin-dependent diabetes. K R Feingold, C Grunfeld, M Pang, W Doerrler and R M Krauss. Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:1496-1502, originally published December 1, 1992).

A common, heritable phenotype characterized by the predominance of small, dense LDL particles (LDL subclass phenotype B) is associated with relatively increased concentrations of plasma triglycerides, reduced levels of high density lipoprotein, and increased risk of coronary artery disease in comparison with subjects with larger LDL (LDL subclass phenotype A).

Further:

The LDL B phenotype was associated with higher plasma triglyceride levels and a trend toward lower high density lipoprotein cholesterol levels compared with the LDL A phenotype in the NIDDM subjects, as has been previously observed in control groups.

Indices of diabetic control, such as fasting and hemoglobin A1 levels, were similar regardless of LDL phenotype pattern, suggesting that glycemic control was not likely to account for the increase in the LDL B phenotype. In both control and NIDDM subjects, the clearance of triglyceride-rich lipoproteins was slowed in the subjects with the LDL phenotype B compared with those with the A phenotype.

The mix of Phenotype A and Phenotype B LDL particles can be determined from other blood numbers (The American Journal of Cardiology Volume 94, Issue 2, 15 July 2004, Pages 219-222. Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Viktor Hanak MD, Julian Munoz MD MSPH, Joe Teague MD, Alfred Stanley Jr. MD. Vera Bittner MD MSPHc):

A triglyceride/HDL cholesterol ratio of 3.8 divided the distribution of LDL phenotypes with 79% (95% confidence interval [CI] 74 to 83) of phenotype B greater than and 81% (95% CI 77 to 85) of phenotype A less than the ratio of 3.8. The ratio was reliable for identifying LDL phenotype B in men and women.

I created an on-line lipids calculator to calculate the number from blood test results.

See also (Why LDL-Cholesterol May Be Overestimated on a Low-Carb, High-Fat (LCHF) Diet).

HyperInsulinemia – Finding the Moving Target

My BLOG posts on hyperinsulinemia.

A related BLOG post by an MD (Hyperinsulinemia: Should You Be Tested?).

My initial target was hacking my diabetes. That was even the subtitle of my original BLOG (Hacking my T2DM). For years, I took the medications that the doctors gave me and my diabetes got worse. In the end I was on 100+ units Insulin delivered via a pump and I was getting worse. I thought there must be a better target since the doctor’s approach wasn’t helping me.

Diabetes and Insulin Resistance

In seeking answers, I found that the diabetes related to Insulin Resistance. So I chased after curing my Insulin Resistance via the Low Carb diet. In doing so my diabetes was apparently cured.

Certainly the low carb diet has greatly helped my Insulin Resistance, but the question remained of whether my diet has cured my Insulin Resistance and there’s indications that I am not completely cured (Insulin Resistance Test).

Aspects of Insulin Resistance

Turned out that Insulin Resistance has a bunch of subtle aspects. There’s hepatic (in your liver) Insulin Resistance, peripheral (in your muscles) insulin resistance, physiological insulin resistance, etc. Each of these play a role in diabetes and each are affected in various ways by the Low Carb diet.

Somebody may have written a good write-up on all of this but I haven’t yet seen it. Everyone seems to have a piece of the story. Perhaps a BLOG post sorting it out would be helpful?

Fatty Liver and Diabetes

Recently, I’ve been circling around a more nuanced view of the problem and have been looking more closely at the role of the fatty liver and glycogen stores.

Your body stores glucose in the liver as glycogen. Once those glycogen stores are filled, excess carbohydrates then fill up the liver fat. . Fat then overflows into other internal organs, particularly the pancreas. Eventually the pancreas isn’t able to make enough Insulin to keep up with the resistant areas. That’s when you end up on insane levels of Insulin.

How Does a Low Carb Diet Work?

Low carb reverses fatty liver quickly by first dropping glycogen stores. It only takes a day or two of eating very low carbs to reduce your glycogen stores to minimal levels.  The liver then mobilizes its own fat for energy. This leads to a leaned liver within a week or less. This leads to less fat in the pancreas and restores normal insulin production in the pancreas.

In addition, the reduction in carbohydrates leads to a reduction in blood glucose and insulin levels. The lower glucose load allows the pancreas to keep up. This is part of why the Low Carb diet is effective with diabetes so quickly.

Obesity fits into this in a strange way since increasing insulin sensitivity (decreasing Insulin Resistance) allows cells to take up more glucose. But a low carb diet reduces the glucose from the diet. Under a low carb diet most of the glucose the body needs comes from Gluconeogenesis (GNG) (glucose made by the liver from stuff other than glucose). So GNG which is a problem under a high carb diet because it contributes to the amount of glucose in the body, then becomes what provides the necessary glucose to survive under a low carb diet.

What Causes What?

But all of this raises the question of what causes what. Current dogma mostly blames energy surplus as the problem. You are fat because you eat too much and getting fat makes you Insulin Resistant, diabetic, etc.

Since the Low Carb cure reduces weight it’s hard to tease out which effect leads in terms of the effectiveness of the cure. I know in my own case that I got off all Insulin within two weeks and I hadn’t lost much weight yet.

The Real Target

I’ve come to view Hyperinsulinemia as the central issue in the development of the cluster of issues known as Metabolic Syndrome (hypertension, hyperlipidemia, obesity, Type 2 Diabetes).  Others have recently presented the same insight. One crucial paper on the subject is (Erion, K.A. & Corkey, B.E. (2017). Hyperinsulinemia: a Cause of Obesity? Curr Obes Rep (2017) 6: 178.).

Purpose of Review

This perspective is motivated by the need to question dogma that does not work: that the problem is insulin resistance (IR).

The prequel to severe metabolic disease includes three interacting components that are abnormal: (a) IR, (b) elevated lipids and (c) elevated basal insulin (HI). HI is more common than IR and is a significant independent predictor of diabetes.

We hypothesize that

(1) the initiating defect is HI that increases nutrient consumption and hyperlipidemia (HL);

(2) the cause of HI may include food additives, environmental obesogens or toxins that have entered our food supply since 1980; and

(3) HI is sustained by HL derived from increased adipose mass and leads to IR.

We suggest that HI and HL are early indicators of metabolic dysfunction and treating and reversing these abnormalities may prevent the development of more serious metabolic disease.

Not only are high levels of Insulin the key driver in the processes related to the development of Metabolic Syndrome but they are the key drivers in reversing Metabolic Syndrome.

Taking exogenous Insulin drives hyperinsulinemia.

Eating too many carbs drives hyperinsulinemia like nothing else can do.

Reversing hyperinsulinemia via a combination of low carb diets and fasting does the best possible of any treatment.

Another view showing evidences on both sides (Shanik MH1, Xu Y, Skrha J, Dankner R, Zick Y, Roth J. (2008). Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care. 2008 Feb;31 Suppl 2:S262-8.).

We examine situations where insulin itself appears to be a proximate and important quantitative contributor to insulin resistance.

1) Mice transfected with extra copies of the insulin gene produce basal and stimulated insulin levels that are two to four times elevated. The mice are of normal weight but show insulin resistance, hyperglycemia, and hypertriglyceridemia.

2) Somogyi described patients with unusually high doses of insulin and hyperglycemia. Episodes of hypoglycemia with release of glucose-raising hormones, postulated as the culprits in early studies, have largely been excluded by studies including continuous glucose monitoring.

3) Rats and humans treated with escalating doses of insulin show both hyperinsulinemia and insulin resistance.

4) The pulsatile administration of insulin (rather than continuous) results in reduced requirements for insulin.

5) Many patients with insulinoma who have elevated basal levels of insulin have reduced (but not absent) responsiveness to administered insulin.

In summary, hyperinsulinemia is often both a result and a driver of insulin resistance.

 

Liver Fat and Low Carb

Here’s a thought that is initially quite scary until you figure out what is going on.

Low Carb Diets increase Liver Fat.

There is a mouse study which shows that Low Carb diets increase liver fat (Curr Opin Clin Nutr Metab Care. 2012 Jul; 15(4): 374–380. Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease. Rebecca C. Schugar).

Mice fed the Ketogenic Diet (KD) for 12 weeks were lean, euglycemic, ketotic, and hypoinsulinemic, but were glucose intolerant, and exhibited NAFLD.

MRS revealed that KD-fed mice accumulate hepatic lipid within 3 weeks after initiation of the diet, and the hepatic gene expression signature for DNL (encoded mediators of SREBP-1c, FAS, ACC1, SCD1) was suppressed compared to livers of chow-fed controls.

In contrast, mice fed the WD ultimately accumulate higher IHTG than KD-fed animals, but do so much more slowly, and as expected due to the high sucrose content, induce mediators of DNL.

So, mice fed the western diet accumulated MORE liver fat over time…

Wait, I thought that’s what you are trying to solve by doing a low carb diet? Yep. Here’s the difference. Here’s a pretty simple explanation (Reddit thread).

Fatty liver in humans is primarily caused by hepatic triglycerides that the liver fails (for whatever reason) to remove from the liver via VLDL or oxidize for fuel. So, if you’re insulin resistant, the liver gets regular and massive influxes of carbohydrate, not to mention an increase in hepatic glucose production that is also characteristic of insulin resistance.

Your body has three options with excess carbohydrates; store as glycogen, burn as fuel, or store as fat. When the carbs are in excess, the first two former options are often impossible, so your body opts to attempt to store carbohydrates as fat. However, if this happens faster than your liver can manage, the triglycerides accumulate. This is just how NAFLD works in humans (Clinical Lipidology, 1st edition, ch. 37, pg 448).