by Catherine M. Haug, January 2007; updated February 2007 and April 2021 [note: red text indicates updates/changes yet to be made]
- Review “articles to study;”
- Diabetes Challenge – Dr MMurray;
- Review “Growth Hormone Replacement Therapy Induces Insulin Resistance by Activating the Glucose-Fatty Acid Cycle.” (ref 22) and add notes to this posting, or create a new post
This article is quite long; consider dividing the following topics into two parts, as indicated:
- Part 1: Intro to IR Causes
- What Causes Insulin Resistance
- Cortisol, Adrenal Fatigue and Insulin Resistance
- Growth Hormone and Insulin Resistance
- The Glycosylation Connection
- Part 2: Fat-Induced Insulin Resistance
- Trans Fats (Hydrogenated and Partially-Hydrogenated Fats and Oils)
- Insulin Receptor Site Integrity
- GLUT Transporter Integrity
- Mitochondria Control of Receptors
- LDL Receptor Site Integrity
- Brown Fat and Post-Insulin Receptor Activity; see also pdf: Adipose Tissue: White and Brown Fat
- Trans Fats (Hydrogenated and Partially-Hydrogenated Fats and Oils)
- See also (this site): 1. Diet and Health Menu*; 2. Notes on Insulin Resistance (IR); 3. Choline, Inositol, and Insulin Resistance; 4. Ketogenic Diet; 5. Cyclical Ketogenic Diet (CKD) and Metabolic Mitochondrial Therapy (MMT)
‘*See Diet and Health Menu under “Insulin, Insulin Resistance, and Metabolic Syndrome” for list of other articles about Insulin Resistance (some still need to be moved to Cat’s Kitchen)
Refer to my article Insulin: Master Regulator to learn more about insulin’s amazing functions, and how it regulates blood sugar.
Articles to study 1. Science Daily: Too Much Protein Along with Fat May Lead to Insulin Resistance (15); 2.related discussion: PaleoHacks.com: High Fat + High Protein = Insulin Resistance (18); 3. MetabolicHealing.com: Purines in Metabolic Typing (19). As I study these, I will add this info.
Part 1: Intro to IR Causes
Dr Michael Murray’s Diabetes Challenge Quiz
From Dr Murray’s email:
“This quiz will help you determine what is your biggest challenge to blood sugar control.
There are 4 specific challenges that can cause your blood sugar to rise and there are specific strategies based on these challenges to bring blood sugar levels down.
Based on your gender, age, body shape and 3 other factors, I can accurately determine exactly which blood sugar challenge is affecting your readings, and give you these results for free.
[There are] 4 challenges: the Thrifty Genotype, exposure to POPs, low AMPk, or high Cortisol.”
To take the 6-question quiz, see the link at reference (20a).
There are several videos in his quiz series, the url of each increases by 1 at the end of each url (i.e. v1, v2, v3, etc).
- I took the quiz, and fall in the first challenge (v1): The Thrifty Genotype; see his 11 minute video (reference 20b) for more about the this type. [Cat’s note: I could have fallen into his high cortisol type because I used to have that problem, but now my cortisol is always too low.
- The second challenge (v2) is 9 minutes (reference 20c).
[Cat’s note: I’d like to copy the following article to this post (or link to it in a new post): See DOCUMENTS > iWEB-HTMTL > Dec2018-HealthDocuSeries > Health Docuseries / DiabetesChallenge-DrMMurray.html]
What Causes Insulin Resistance?
Many people believe that the over-consumption of processed sugars, lack of exercise, and/or obesity causes Insulin Resistance (IR), and indeed, may be factors. But might this not be putting the cart before the horse? It could be that Insulin Resistance causes such extreme cravings for sweets, that the person is unable to resist and thus over-consumes, becoming an obese couch potato. Or the Insulin Resistance could directly lead to obesity, even without over-consumption.
Many practitioners believe that elevated blood insulin makes the cells resistant to it, but if this is true, what causes the serum insulin levels to rise in the first place? Is the insulin defective? No; research indicates that there is no change in the insulin. Is the sugar defective? No; the glucose is still glucose. The only other explanation is that something is wrong in the cells or their environment to make them insensitive; related to this are the hormones that regulate your body’s function and metabolism, including cortisol, insulin, leptin and thyroid hormones.
In other words, insulin resistance gives rise to elevated blood insulin, not the other way around. When cells become insulin resistant (but those same cells still have a need for a particular nutrient regulated by insulin) the pancreas produces more insulin, leading to elevated blood insulin levels.
What causes insulin resistance: It all boils down to your diet: The kind and amount of fats, carbs and protein you consume. One author suggests the following in each category to reverse insulin resistance and burn the fats stored in your fat cells* (17) [Cat’s note: that author is trying to sell you his product which contains his recommended foods; there are many other good foods in each category as well.]
Medium-chain fatty acids, such as those found in coconut oil or manufactured MCT oil. [Cat’s notes:
- I’d much rather eat natural coconut oil, than manufactured MCT oil.
- Another source of MCTs is raw or simply pasteurized dairy milk (not ultra-pasteurized), or the cream, butter or ghee from this type of milk. The short-chain fatty acids such as those found in these products are also good for you, but you don’t generally burn those for energy; instead, the microbiome in your gut converts them to other healthful substances.NOTE: ultra-pasteurized milk or milk products do not provide these benefits because the ultra-pasteurizing process damages the nutrients.
- Other good fat sources include pure olive oil, cod liver oil, wild-caught salmon and sardines, duck and goose fat, avocados, flax seeds (freshly-ground), eggs, and nuts.]
Meat vs plant-based protein. A Mercola article (26) discusses research on this topic, with the conclusion:
- “consuming meat does not lead to increased inflammation or oxidative stress, but improves insulin resistance and insulin sensitivity.“
- “A study published in the Journal of Nutrition, in which 60 people partially replaced carbohydrate-rich foods in their diet with 8 ounces of lean red meat daily for eight weeks. Markers of oxidative stress and inflammation did not increase and, in fact, CRP, a marker for inflammation in the body, decreased. Markers of insulin resistance and insulin sensitivity also improved
Good Proteins: wild caught salmon or dairy whey. Wild caught salmon is far better than farmed salmon for many reasons, including the type of fat in the meat. Dairy whey is found in quality dairy milk and mother’s milk. [Cat’s notes:
- Other excellent sources of good protein are bison, lamb, venison, goat, and beef from animals raised and finished on pasture.
- Also raw or simply pasteurized dairy milk, eggs from pastured hens, and sprouted dried beans/peas.]
Sweet potatoes, winter squash, wild rice, brown rice and black and other fresh or dried beans (preferably sprouted) are examples of good high-carb foods. [Cat’s notes:
- because brown (and white) rice are high in toxic arsenic, I recommend wild rice.
- Greens such as kale, broccoli, spinach, beet greens, chard, and parsley are also good carbs because they provide good fiber.
- Beets are also great, especially when fermented.]
The above lists of dietary choices can also be found on Cat’s Kitchen: Good Foods to Fight Insulin Resistance and Overweight
Cortisol, Adrenal Fatigue, and Insulin Resistance
Blood Sugar Imbalance and Diabetes
From Today’s Nutrition, Nov 2009, Cortisol — Its Role in Stress, Inflammation, and Indications for Diet Therapy, by Dina Aronson, MS, RD (21a):
“Under stressful conditions, cortisol provides the body with glucose by tapping into protein stores via gluconeogenesis in the liver. This energy can help an individual fight or flee a stressor. However, elevated cortisol over the long term consistently produces glucose, leading to increased blood sugar levels.
Theoretically, this mechanism can increase the risk for type 2 diabetes, although a causative factor is unknown.(21b) Since a principal function of cortisol is to thwart the effect of insulin—essentially rendering the cells insulin resistant—the body remains in a general insulin-resistant state when cortisol levels are chronically elevated. Over time, the pancreas struggles to keep up with the high demand for insulin, glucose levels in the blood remain high, the cells cannot get the sugar they need, and the cycle continues.
Elevated cortisol also increases inflammation and suppresses immunity; can cause gastrointestinal problems (primarily by causing inflammation), compromising digestion and absorption. (21a)
From Insulin Resistance: A Weighty Matter (16):
“Cortisol, which is produced by the adrenal glands, reduces insulin’s ability to carry glucose into cells. Stress raises cortisol levels, triggering the release of stored sugar as part of the “fight or flight” response. Chronically high levels of cortisol contribute to insulin resistance and may also explain why some insulin-resistant people report unexplained feelings of alarm or anxiety.” …
“Low testosterone and progesterone levels may also lead to insulin resistance in both men and women. Michael E. Platt, MD, author of The Miracle of Bio-identical Hormones maintains that the major cause of hyperinsulinemia (too much insulin) is too little progesterone. ‘Low progesterone levels,’ he writes, ‘cause over-production of insulin, leading to hypoglycemia and an outpouring of adrenaline to bring sugar levels up.’ According to Dr. Platt, natural progesterone reduces insulin and regulates blood sugar levels.”
Growth Hormone and Insulin Resistance
I don’t yet know much about this (as of 2007 writing of this article), but apparently growth hormone (GH) is involved in insulin resistance. When this hormone is administered to patients, serum insulin rises, indicating an insensitivity of cells to insulin (insulin resistance).(10) The mechanism of this action is not known, but one article asserts it may be related to a commonality in activities after binding of hormone to receptor has occurred. That is, both insulin and GH receptors use the same signaling molecules within the cell, and thus compete with each other. (12)
IGF-I (Insulin Growth Factor – I), a polypeptide with structure similar to insulin, and known to bind to insulin receptors as well as IGF-I receptors, regulates cell growth and development, and DNA synthesis. It has been shown to enhance insulin sensitivity in diabetic patients, in part by suppressing GH. (12)
Another article bears reading, but I’ve not yet gotten to it: “Growth Hormone Replacement Therapy Induces Insulin Resistance by Activating the Glucose-Fatty Acid Cycle.” (22) [Cat’s note: the original JCEM url for this article is no longer valid.].
The Glycosylation Connection
It has long been thought that the enzymatic attachment of sugar to protein, i.e., glycosylation, could only happen to proteins on the cell surface, as those proteins become exposed to sugars in the plasma. But recent research shows that proteins inside a cell can also become glycosylated with simple sugars; indeed, this is a normal process used by cells to control protein activity, including the messenger proteins that relay the insulin-initiated signal to transport glucose into the cell.
One such simple sugar used within the cell is O-linked beta-N-acetylglucosamine, or O-Glc-NAc for short [Cat’s note: N-acetylglucosamine is also known as NAG]. This sugar is made from glucose remaining in the cell (via the hexosamine pathway) after all that was needed for energy has been used (via the glycolytic pathway). It can also be made from glucosamine. Both O-Glc-NAc and glucose can be glycosylated to proteins in the cell via one enzyme, and removed via another enzyme. (3)
When researchers selectively blocked the enzyme that removes O-Glc-NAc from proteins, so that the proteins could be loaded up with that sugar, the affected cells became insulin resistant. These researchers were able to isolate two proteins that were more glycosylated than others [beta-catenin and insulin receptor substrate-1 (IRS-1)], and both are involved in message-relay to uptake glucose from the extracellular fluid. (3)
A 2004 British study of human cultured L6 muscle cells concluded: “Glucosamine decreased insulin-stimulated glucose uptake by L6 muscle cells, providing a potential model of insulin resistance with similarities to glucose toxicity. Insulin resistance induced by glucosamine was not reversed by three agents (metformin, peroxovanadium and d-pinitol) known to enhance or partially mimic the effects of insulin.” (5)
Their conclusion? Glucosamine decreases insulin sensitivity (increases insulin resistance) by inhibiting the action of protein messengers used to relay the insulin-initiated glucose-uptake signal. This could well be the mechanism cells use to turn off glucose uptake, when the cells have enough sugar. And it explains the observation that glucosamine is 10-times as potent (for causing insulin resistance) as glucose in animals. It also serves as a caution to humans who are insulin resistant, to avoid use of glucosamine, as it can increase fasting blood sugar and worsen glucose tolerance. (4)
Cat’s Update: The conclusion that NAG decreases insulin sensitivity has been refuted by Mayo Clinic (24) and Diabetes Library (25), based on more recent studies. See also my article catsfork.com/CatsKitchen/insulin-resistance-leptin-and-lectins/ for more about this.
Part 2: Fat-Induced Insulin Resistance
Now, that’s a mouthful; what does it mean? In a nutshell, when plasma triglycerides (TGs) increase, glucose uptake (in muscle cells) decreases. This is an active area of research, trying to understand the mechanism at the cellular level.
Nearly 100 years ago, it was noted that salicylate (related to aspirin) reduced the severity of glycosuria (the excretion of glucose into the urine) in diabetic patients; a 1957 study demonstrated that 10-14 days of aspirin treatment improved oral glucose tolerance tests in diabetic patients. More recently, researchers discovered that fat-induced insulin resistance in mice could be diminished by salicylate therapy. This led to the hypothesis that a surplus of fatty acids depresses the activity of IRS-1 messenger protein by inhibiting an enzyme responsible for activating this messenger. The IRS-1 protein is part of cells’ signaling mechanism that lead to the uptake of glucose into the cell. (6, 7)
A reader of this site sent me an interesting article from Science Daily (Too Much Protein, Eaten along with Fat, May Lead to Insulin Resistance) 15, on a study that showed when fed proteins high in BCAAs along with plenty of fat, rats developed insulin resistance. As I ponder this, I come up with the following. It refers to P-types (or Protein-types) which are discussed in my articles on Metabolic Types and on Fast Oxidizers in particular:
The metabolic preference of Protein-types for fat and protein to produce energy explains how they become ‘fast oxidizers’ and ‘insulin resistant,’ when they have an abundance of carbs and insufficient protein and fat in their diet. The abundance of sugar from carbs reduces the cells’ sensitivity to insulin, but because they don’t have enough fat and protein to burn, they start craving sugars. They eat more than they need so the liver goes into overdrive to convert the excess sugar into fat for storage in the belly.
At some point, something changes in the liver so that it starts storing this sugar-source fat (‘fatty liver disorder’). This in turn leads to the medical condition known as ‘insulin resistance’ because the liver knows it is processing too much sugar. As far as I know, the mechanism for how this happens is not yet elucidated. Meanwhile, their metabolism speeds up because of the sugar, and this means they become f’ast oxidizers’. Unfortunately, the cravings for sugar don’t stop, which exacerbates the problem.
Trans Fats (Hydrogenated and Partially-Hydrogenated Fats and Oils)
Dietary trans fats lead to the following factors known to increase inflammation and oxidative damage to the endothelial cells lining artery walls:
- increased serum LDL,
- increased inflammation-causing prostaglandins (those made from Omega-6 fats), and
- decreased anti-inflammatory prostaglandins (those made from Omega-3 fats).
Inflammation can lead to many of the problems associated with Syndrome-X (a.k.a. Metabolic Syndrome):
- coronary heart disease,
- obesity, and
- type-II diabetes.
What is really exciting is that this problem may be totally reversible!
There is significant evidence that the ingestion of hydrogenated and partially-hydrogenated fats (trans fats), at the expense of natural cis fats from which they are made, leads to problems at the cellular and molecular level, to make cells resistant to insulin. (14) [Cat’s note: “cis” means that the carbon chains on both sides of the double-bond are on the same side, making a U-shape at the double bond; “trans” means those chains are on opposite side, making a zip-zag shape. See Wikipedia for more, including diagrams (23a).]
To understand this assertion, let’s review what happens when the brain detects an excess of sugar (glucose) in the blood (such as after a meal). (9)
- Pancreas releases insulin into the blood stream.
- If the cell is:
- hungry for glucose, it turns its insulin receptors “on;” insulin binds to receptor, initiating the glucose-uptake process. GLUT transporters inside the cell captures the glucose (at the surface of the cell) and carries it back into the interior of the cell.
- has enough glucose, it turns the receptors “off;” insulin cannot bind to that cell. That is, the cell is insensitive to the insulin (insulin resistant), and the glucose-uptake process is not initiated. This is a NORMAL function of the cell, to protect the cell from the toxic effects of too much glucose.
This process allows several places for things to go awry:
- Signaling from brain to pancreas;
- Integrity of the insulin molecule (this has been shown not to be a factor);
- Integrity of the cell membrane as a whole (1a); 4
- Integrity of the insulin receptor site on the cell membrane (2);
- Integrity of the protein messengers and related enzymes within the cell (post-receptor activity);
- Integrity of the GLUT transporter (9);
- Integrity of the mitochondrial function, and control of insulin receptors. (13)
All of these can be influenced by the substitution of natural (bio-active) fats with synthetic dietary trans fats at the molecular level (as discussed in this Trans Fats section).
Insulin Receptor Site Integrity
Cell membranes are comprised primarily of fats and proteins (as discussed in this Trans Fats section). The fats (as phospholipids) can be saturated, mono-unsaturated, or polyunsaturated, depending on the need of that particular cell, and on what is available. Cell membranes are very dynamic, and there is a high turnover of fatty acids in the cell membranes.
Many of these fats can be manufactured by the body from other fats, or from sugars; but some, the so-called “essential” fats, must be provided by the diet (refer to Essential Fats for more detail):
- linoleic acid (Omega-6); and
- linolenic acid (Omega-3).
Both of these fatty acids contain 18 carbons, and are polyunsaturated; linolenic acid comes in two forms: alpha linolenic acid and gamma linolenic acid. In their natural state (cis), they are bioactive, meaning they have biological function in the living organism. But in their unnatural, hydrogenated state (trans), they lose their bioactivity and act as inhibitors to biological function. See Wikipedia for diagrams of these fatty acids (23b, 23c).
Some of the proteins (in the cell membrane) act as receptors, which bind specific substances to interact with the cell; for example, the insulin receptors. These receptors depend on the neighboring phospholipids to act properly (it’s a spatial or geometry thing).
When man-made, non-bioactive (trans) fatty acids get incorporated into the cell membrane (in place of their natural, bioactive, cis, counterparts), they interfere with receptors on the cell membrane, such as the insulin receptors. (8) Such receptor cites CANNOT FUNCTION as insulin receptors, effectively turning them ‘off.’ While this scenario mimics the natural insulin resistance of cells that already have enough sugar, this impaired cell is deprived of needed sugar, and it continues to call for more insulin. (1, 2) Blood insulin and glucose levels rise, eventually to unhealthy levels. It’s a sad and deadly breakdown of communication.
(refer to my ” Insulin: Master Regulator” article for more on how these receptors work.
GLUT Transporter integrity
The incorporation of trans instead of cis fatty acids into the cell membrane could also decrease the integrity and effectiveness of the glucose transporters (such as GLUT-4), with the same end result: rise in blood insulin and glucose levels and the resultant toxic effects of both. (1)
Mitochondria Control of Receptors
People with IR have about half as many glucose receptors as healthy people, making them much less able to react to insulin. The reason for this is not clear, but one proposal is that the mitochondria, which are responsible for determining when more receptors are needed, are compromised by the presence of trans fats in their complex membrane system (as discussed in this Trans Fats section, above). (1)
LDL Receptor Site Integrity
A similar scenario can be described for LDL (cholesterol) receptors: if non-bioactive (trans) fats get incorporated into the cell membrane in place of their natural, bioactive (cis) counterparts, they could interfere with the LDL receptors, inhibiting cholesterol from being taken into the cells, and thus build up in the blood. This could explain the high serum LDL observed in people with IR.
However, these scenarios also provide HOPE. Whatever the mechanism for HOW trans fats affect insulin sensitivity, elimination of these in the diet should, over time, help the body to recover from this devastating problem. All body tissues rebuild themselves; plasma membranes are especially dynamic. If the source of hydrogenated (trans) fats is stopped, and adequate natural, essential fats are provided in the diet, the cellular and/or molecular situation can be restored to normal. In the case of the scenarios proposed above, cell membranes can be repaired with bio-active fatty aciids, and normal blood sugar regulation can resume. For more information on this hope, refer to the Healing Matters website, or to my essay onInsulin Resistance:Controlling and Reversing.
Brown Fat and Post-Insulin-Receptor Activity
I wrote an article for my old iWeb site on Brown Fat, which I’ve turned into a downloadable pdf: Adipose Tissue: White and Brown Fat.*
Here’s a copy of some of the text from that original article, below. NOTE: the referenced links have been added to a separate list in the References Section of this article, as: BF2, BF4, BF5
- Brown fat is abundant in many newborn or hibernating mammals. It is called “brown” because it is rich with blood capillaries and mitochondria, giving it a rusty or brown color. (BF2) Brown fat is related to muscle tissue.
- Its purpose is to burn energy and generate heat in response to cold or excess calorie intake. (BF5) Brown fat is activated when the body is exposed to cold temperatures, boosting the metabolic rate to warm the body. Taking a daily cold shower might help one lose weight.
- When brown fat is present, excess dietary fuels can be burned to produce heat, rather than stored as white fat. White fat is what accumulates under the skin, leading to obesity.
- Researchers at Joslin Diabetes Center and Children’s Hospital Boston developed cell lines of precursor cells that give rise to brown fat in mice. Then, in 2005, they studied the effect of insulin on these preadipocytes to convert them to brown, rather than white, fat cells. This led to their discovery of a group of genes that govern the genesis of brown fat. Through genetic manipulation, they developed preadipocytes that could not form brown fat. This led to several discoveries, including:
- Insulin-resistant cells lacking in IRS-1 (Insulin Receptor Substrate-1) failed to develop into mature brown fat cells; restoring the IRS-1 mostly restored the ability to form brown fat cells.
- Elevated production of a protein called “necdin” inhibits the ability of preadipocytes to form brown fat cells.
- A transcription factor called CREB is essential for reducing necdin production. (BF4)
- This research is opening the doors for development of drugs to fight obesity. But to me, this research is a very important factor in the accumulated knowledge about insulin resistance (IR), which is behind the set of disorders collectively termed Syndrome-X or Metabolic Syndrome. Rather than fighting obesity by suppression mechanisms (drugs), wouldn’t it be better to work on the underlying problem of insulin resistance?
‘* Pdf saved: CATSFORK-ESP-Web > CATSFORK-QTH > PDF Files / AdiposeTissue-White-and-Brown-Fat_042121
Many causes of IR have been proposed; the most likely involve problems at the cellular level.
In my case, I believe adrenal fatigue, along with over-consumption of simple sugars when I was in my 20s-30s, and insufficient inositol in my diet are the main factors.
Man-made hydrogenated trans and interesterififed fats, which were introduced to the American consumer shortly before the new disease called adult-onset diabetes (type-2) appeared on the scene, seem to be the most likely culprit responsible for this disorder, now occurring at epidemic proportions.
- Part 3: Insulin Resistance; Controlling and Reversing
- Insulin: Master Regulator for more on insulin’s amazing functions
Sources and References:
- healingmatters.com/ (note: these links are not secure); specifically, thefollowing:
- hopkinsmedicine.org/news/media/releases/molecular_link_between_high_glucose_metabolic_disease_may_offer_new_strategies_to_control_diabetes (replaces the original link)
- verywellhealth.com/side-effects-of-glucosamine-88199 replaces the original link: altmedicine.about.com/cs/arthritis/a/Glucosamine.htm
- pubmed.ncbi.nlm.nih.gov/15171754/ is better than the original link which is no loner valid Glucosamine-induced insulin resistance in L6 muscle cells
- Prevention of fat-induced insulin resistance by salicylate by Kim, et.al (www.jci.org/cgi/content/full/108/3/437)
- Thieme-connect – Abstract: (https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-2004-819214) (original link was replaced by this new link format)
- pubmed.ncbi.nlm.nih.gov/15539203/ replaces original link: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15539203&dopt=Citation, J. Nutr. Biochem, April 1990, by D.E. Barnard, et.al.
- http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/pancreas/insulin_phys.html< I can’t get this link to open (4/16/21)
- Caution: insecure link: findarticles.com/p/articles/mi_m0DED/is_8_19/ai_54219760
- jcem.endojournals.org/cgi/content/abstract/87/9/4356 < this link is no longer valid; it simply pulls up the Endocrine Society home page
- Journal of Clinical Investigation articles:
highbeam.com/doc/1G1-85522983.htmllink no longer valid; possible replacements:
- The Type 2 Diabetes Breakthrough, a book by Dr. Shallenberger (See AMAZON ISBN-10: 1591201268 or ISBN-13 : 978-1591201267.
- Insulin Resistance: A Weighty Matter: https://collierdrug.com/wp-content/uploads/2015/12/Insulin-Resistance-A-Weighty-Matter.pdf [original link no longer valid
- simplefatfix.com/news/1108/letter; note: this is a sales pitch for his product
paleohacks.com/questions/126511/high-fat-high-protein-insulin-resistancelink no longer valid; can’t find replacement
- Dr Murray:
- For his quiz: doctormichaelmurray.clickfunnels.com/blood-sugar-quiz-optin14371077 (original link no longer valid); and for more detail:
- Today’s Dietician (TD) and their references:
- (TD’s ref 1) Andrews RC, Herlihy O, Livingstone DEW, Andrew R, Walker BR. Abnormal cortisol metabolism and tissue sensitivity to cortisol in patients with glucose intolerance. J Clin Endocrinol Metab. 2002;87(12):5587-5593.
- academic.oup.com/jcem/article/88/4/1455/2845123 (old link was : jcem.endojournals.org/cgi/content/full/88/4/1455)
- Mercola: articles.mercola.com/sites/articles/archive/2021/04/24/experts-face-off-plant-based-versus-meat-based.aspx
Links from iWeb article on Brown Fat (BF-numbers in parenthesis are from that article):