Does Saturated Fat Cause Insulin Resistance? | DRS 188


When does menopause startIn this episode of The Dr. Rob Show we discuss a quesiton set in by a listener, concered if saturated fats can cause insulin resistance.

Discuss levels of IR: (include Metabolic Syndrome)

  • Low, moderate or high risk
  • Download IR risk assessment from content library


Types of Fats:

  • Saturated
  • Polyunsaturated
    • Omega 3
    • Omega 6
  • Mono-unsaturated
    • Omega 9


Type of Fat


Bad (trans)


Butter (grass-fed)

Heavy Cream (grass-fed)

Coconut oil


Beef tallow (grass-fed)

Crisco (shortening)

Palm oil


Cod liver oil

Fish oil

Flax oil

Borage oil

Evening primrose oil

Grapeseed oil


Corn oil

Vegetable oil

Soybean oil

Canola oil

Safflower oil


Monounsaturated Olive oil


What are Trans Fats? 

  • Fats in general are very susceptible to heat, which changes the chemical structure of the fat molecule from a Cis conformation to a Trans conformation.  By changing the confirmation to trans, the fat does not go rancid and will increase shelf.

Fat storage, loss & Metabolism:

  • Carbohydrate ingestion are broken down into glucose
  • Lipogenesis at the fat / adipose cell turns the glucose into fatty acid and glycerol and then into triglyceride thus increasing the fat cell
  • This fat storage from eating carbohydrates is based on insulin
  • Insulin is released from the carbohydrate. The amount of insulin released is based on the type of carbohydrate consumed
  • Insulin inhibits hormone-sensitive-lipase, which this causes the weight gain
  • Fat ingested becomes chylomicrons which at the fat/adipose tissue by way of lipoprotein-lipase become glycerol+fatty acid and converts to triglycerides to be stored as fat
  • So in theory, too much fat can cause weight gain
  • There is no insulin release with ingestion of fat only
  • Fat has a GI / GL of zero
  • Meaning, fat does not cause insulin resistance, nor does it lead to diabetes
  • But, fat in excess can cause weight gain – Maybe?
  • Fasting:  In the presence of cortisol will cause growth hormone to increase
  • Lipolysis breaking fat / triglycerides into glycerol and fatty acid (glycerol will go to the liver)
  • By way of gluconeogenesis will be converted to glucose for the brain
  • The fatty acid will then be available to the blood for the heart, muscle
  • Short term fasting–not eating for a few hours: In the presence of cortisol, epinephrine and norepinephrine is released
  • These catecholamines promote lipolysis to breakdown the triglyceride in the fat cell into glycerol and fatty acid

Do saturated fats cause insulin resistance?


  • There are some studies to suggest that saturated fats cause insulin resistance.
  • Is there any validity to this idea?
  • Fats in general have been vilified for 50 years as the major
  • Denise Minger’s book “Death by Food Pyramid”
  • Research study design flaws
  • Fed fat and carbs (rat chow)
  • Talk about Valorie’s lab experience
  • Rats with genetic predisposition to IR and diabetes
  • Fat by itself has 0 GI
  • Fat + carbs causes a greater insulin response, thus leading to IR
  • However, a high fat diet for a Diabetic might not be good because of the presence of higher insulin levels, then a non-diabetic
  • Loren Cordain (Paleo Diet)
    • Hunter Gather tribes around the world
    • Diets consist of mainly saturated fats and vegetables
    • About 58% from fat and 30% from carbs and the rest from protein
  • Ceramide formation in cell membranes, correlated with dietary saturated fat intake  Ceramides are fatty acid and sphingomyelin molecule that impair insulin signaling
    • LPS (endotoxin) found to promote ceramide formation
    • Cortisol also promotes ceramide formation


A Solution for Insulin Resistance


When does menopause start

In this episode of The Dr. Rob Show, we continue our series on insulin resistance and weight gain and discuss a simple solution for this very common issue.  With the stresses of everyday life, losing weight can be very difficult.

The key to weight loss success is consistency and time, there is no magic bullet or a way to speed up the process without negative consequences.  The strategy someone implements needs in order to lose weight needs to simple, easy to follow and the most important is it needs to be maintainable over time.

The IR Solution is based on the concept of Intermittent Fasting and is a simple, but effective strategy to implement that can help in the weight loss process.

Hormones that affect weight gain:

  • Insulin
  • Cortisol
  • Leptin
  • Ghrelin
  • Thyroid
  • Sex hormones

In addition to hormones, new research is pointing towards the role the microbiome plays in the weight gain and insulin resistance process.

Quick overview of solution: 

  • Breakfast will be fat only
  • Lunch will be protein + fat
  • Dinner will be protein + starchy carbohydrate
  • Eat lunch and dinner in a 6-8 hour window
  • Ex: eat lunch at noon and dinner between 6:00 and 8:00 pm
  • You will be fasting for 16-18 hours per day

The key to remember is your body burns what you give it, so by having fat first thing in the morning, it encourages the body to burn fat efficently.  Plus, having a decent amount of healthy fats in the morning helps to improve energy, manage appetite and minimize cravings later in the day.  Having carbs with dinner helps to improve the quality of sleep and makes it more maintainable.

To get you copy, visit and join the community where you can download the IR Solution from the content library.



Are You Insulin Resistant? | DRS 186


When does menopause startWhat is insulin?

  • Insulin is a hormone that is secreted from your pancreas
  • It is secreted to help the body manage glucose.
  • When we eat something that has sugar in it (carbohydrate–complex or refined), the blood sugar (glucose) rises in your blood stream
  • The pancreas then secretes insulin in response to the rise in blood glucose.  Insulin allows glucose to enter cells
  • In diabetes type I the beta cells of the pancreas are destroyed, which means there is no insulin released in response to blood sugar
  • Diabetes Type II is a completely different then Type I

Destinations of glucose from carbohydrates: 

  • Burn as fuel
  • Store as glycogen (liver and muscle)
  • Store as fat
  • Make cholesterol

Key notes to remember:

  • Insulin is a fat storing hormone, so that means more insulin more fat storing
  • Amount of insulin secreted from pancreas is where the pathology begins
  • Insulin is meant to help:
    • in the formation of energy for use now
    • storing “energy”, aka fat. (from too many carbs)
    • keep the blood sugar in a proper healthy range
  • The amount of insulin secreted is very important as in the short term.  Too much insulin will cause reactive hypoglycemia and storage of fat
  • In the long-term, too much insulin released over time will cause insulin-resistance.
  • The insulin receptors on cells will become resistance to the message of insulin–causing glucose not to be allowed to enter the cell resulting in high blood glucose.  Over time this will lead to diabetes type II
  • Receptors will actually “down-regulate,” or decrease in number

How does one develop hyperinsulinemia?

  • Foods with a high glycemic load
  • Foods / meals with a high glycemic index
  • Our paleolithic ancestors ate 22 teaspoons of sugar a year in the form of natural sweeteners.  By 1800, the average person consumed 10 pounds of sugar a year
  • Current sugar consumption is 150-180 pounds per year, per person (half a pound a day)
  • Nutrient density–fiber content: paleolithic fiber consumption was 100 grams a day, vs it is less than 8 grams per day
  • Artificial sweeteners have been shown to increase hunger

Hyper-insulinemia–high insulin also causes:

  • Wanting to eat more frequently
  • Greater appetite / cravings
  • Weight gain, especially in the stomach
  • Inflammation
  • Immune dysfunction


  • Chronic stress drives chronically elevated cortisol.  Chronically elevated cortisol promotes insulin resistance, belly fat
  • It also interferes with testosterone production, thyroid and growth hormones
  • Also cortisol interferes with sleep patterns which alters hormone function and causes weight gain
  • Sleep: sleep deprivation and impaired sleep increases cravings for sugar and carbs as well as promotes weight gain in the stomach
  • Insulin resistance also affects fertility, the immune system, increases inflammatory reactions
  • One of the most serious consequences of insulin-resistance is it is a prelude to Type II Diabetes
  • If you have IR, and do not make the appropriate changes, you will get diabetes

What is Metabolic Syndrome? 

  • Increased visceral adipose fat (belly fat):
    • Waist circumference > 40 inches men
    • Waist circumference > 35 inches for women
  • Fasting blood sugar greater than 100
  • Triglycerides greater than 150.
  • Reduced HDL < 40 HDL men and < 50 HDL women
  • Increased blood pressure 135/80
  • Insulin resistance causes metabolic syndrome

What is the difference between Insulin Resistance and Metabolic Syndrome?

  • Insulin resistance and metabolic syndrome cannot be separated
  • In our opinion, Insulin Resistance is the precursor to Metabolic Syndrome

Gut Microbiome:

  • The connection between digestion, immune system and endocrine system
  • Leaky gut, SIBO and dysbiosis leads to inflammation
  • Increase in inflammatory cytokines which leads to Insulin Resistance
  • Leaky Gut → Inflammation → Insulin Resistance


What is Leptin Resistance? | DRS 185


When does menopause startIn this episode of The Dr. Rob Show, we discuss some of the hormones that control appetite and help the body gain and lose weight.  Obesity occurs when this hormone system becomes imbalanced.


  • Produced by adipose/fat cells.
  • Hormone that binds to receptors in the brain for appetite.
  • Leptin also stimulates adipose/fat burning.
  • Leptin will tell the brain/hypothalamus that you are hungry or you are not hungry. So in theory, the more fat we carry, the more leptin is produced telling the brain that we are satiated.
  • Or if we do not have enough fat stores, therefore we will have lower leptin and this low leptin signals the brain that we have an appetite.
  • “Leptin Resistance”
  • This is where this system is not working.  There is fat stores and plenty of leptin but the appetite is not satiated.  In fact, the in “leptin resistance” there is increased hunger and hence more weight gain.
  • Actually, in obesity the brain thinks that the body is starving because it is not receiving the high leptin signals.
  • Cutting calories is not going to work in this instance.  It will make you more ravenously hungry is you think you are leptin resistant and reduce your calories.
  • Reducing calories does not reverse Leptin Resistance.
  • This system is still in science unclear–but it is being found out that leptin may control ghrelin.
  • Leptin resistance and insulin resistance usually occur together.  People with insulin resistance have leptin resistance.


  • Fast-acting hormone that is released from the lining of the stomach and stimulates the brain/hypothalamus.
  • It is released when your stomach is empty.
  • Ghrelin is high before a meal so that your appetite increases and you go looking for food and lower after a meal when your stomach is full.
  • When you have not eaten for a while, then your stomach will release the ghrelin which will them stimulate your brain and tell you that you are hungry.
  • Ghrelin increases appetite.
  • Leptin decreases appetite.
  • Leptin resistance means the brain is not responding to the high levels of leptin, in effect the brain “thinks” the leptin is actually low.  Hence, the mechanism to
  • “decrease appetite” is turned off.  As well as the mechanism for increased fat burning.  Remember, leptin also increases metabolism to an extent.
  • Reducing calories and not eating to lose weight is going to increase ghrelin.
  • So lets say you are overweight which leads into leptin resistance.
  • This leptin resistance is going to shut off the “appetite suppression”, leading you to be hungry and tired because of the reduced metabolic activity.  Now you are gaining more weight.
  • So you go on a “diet” and cut your calories and stop eating. Now your ghrelin is going to go up increasing your appetite even more.  That is why diets do not work–go on a diet if you want to gain weight.
    • Increase Fat
    • Increase Protein
    • Reduce refined carbohydrates and sugar
    • Do not cut your calories
    • Sleep –good sleep reduces ghrelin
    • Exercise
    • Gut-biome


  • Adiponectin is a protein involved in regulating glucose levels as well as beta oxidation, which the process of burning fat.
  • Females have higher levels of adiponectin than males.
  • Adiponectin is released from adipocytes-specific, which is suggested to play a role in the development of insulin resistance and atherosclerosis.
  • The primary mechanisms by which adiponectin enhance insulin sensitivity appears to be through increased fatty acid oxidation and inhibition of hepatic glucose production.
  • Levels of the adiponectin are inversely correlated with body fat percentage in adults, which means the fat you have the lower the level of adiponectin.
  • Pro-inflammatory cytokines especially tumour necrosis factor-alpha can decrease adiponectin levels.
  • Circulating adiponectin concentrations increase during periods of caloric restriction.
  • Adiponectin exerts some of its weight reduction effects via the brain, which is similiar to the action of leptin, but the two hormones perform complementary actions and can have synergistic effects.

Adiponectin effects:Glucose regulation

  • Decreased gluconeogenesis
  • Increased glucose uptake
  • Beta oxidation (fat burning)
  • Increased insulin sensitivity
  • Protects against endothelial dysfunction, which is an important factor in the development of atherosclerosis
  • Reduction of TNF-alpha, which is an pro-inflammatory cytokine

Regulation of adiponectin

  • Obesity is associated with decreased adiponectin.
  • The exact mechanism of regulation is unknown, but adiponectin could be regulated by post-translational mechanisms in cells.

Possible Testing Options:

  • Insulin, fasting
  • Insulin x 4 (post-prandial)
  • Lipids
  • Liver enzymes ?
  • Leptin
  • Adiponectin
  • Cortisol, total / 24 hour urine (subclinical Cushing’s ?)
  • TSH
  • Free T3
  • Free T4





What is SIBO? – Digestive Series Part 3 | DRS 184


When does menopause startIn this episode of The Dr. Rob Show, we contiue with part 3 of our digestive series and discuss SIBO and Dysbiosis.

What is SIBO? 

  • SIBO: Small intestinal bacterial overgrowth
  • Small intestines is made up of the duodenum, jejunum, ileum
  • Jejunum and ileum is where nutrients are absorbed
  • Small intestines also produces nutrients such as vitamin K and folate.
  • There is not suppose to have any  a lot of bacteria in the the small intestines.  SIBO is when bacteria from the colon backs into the small intestines. The connection of of the small intestines into the large intestines is the ileocecal valve.  If this valve allows bacterial from the colon into the small intestines, this creates SIBO.
  • SIBO is where there is a increase in bacteria (overgrowth) as well as inappropriate bacteria from the colon enters the small intestines.
  • What happens when there is bacterial from the colon into the small intestines and overgrowth?
  • Destroy the lining of the small intestines which makes it “leaky” –leading to Leaky-Gut aka increased intestinal permeability.
  • Lead to nutritional deficiencies as well as reduced absorption.

Symptoms of SIBO: 

  • Bloating
  • Stomach pain
  • Bowels disturbances
  • Gas
  • Belching
  • Leaky-gut
  • Food intolerances/sensitivities
  • Fatigue
  • Brain-fog
  • Anemia
  • Cannot tolerate probiotics

Causes of SIBO: 

  • Medications: antibiotics, reflux meds, antacids
  • Diet inflammatory diet
  • Low stomach acid–meds or otherwise
  • IBD
  • Hormonal imbalances
  • Lab testing/diagnosis: available on our website as conventionally this is not common practice
  • Breath test:
    • Testing hydrogen and methane


  • Common treatment is Rifaximin (antibiotic)–recurrence is very common
  • Antimicrobials
  • Dietary changes:
    • Non inflammatory diet
    • Low in sugar
    • Low refined carbohydrates
    • Low in alochol
    • 4 Rs: work on digestion

What is Dysbiosis: 

  • We have lots of bacteria in the colon–symbiotic relationship
  • Beneficial bacteria
  • Pathogenic bacteria and yeast
  • Dysbiosis is when the beneficial bacteria is being outnumbered by the pathogenic bacteria and yeast.
  • Beneficial bacteria: keeps acidic environment of the colon 6.7-6.9 pH
  • Pathogenic bacteria and yeast
    • Yeast candida
    • salmonella, shigella, C. diff, E.coli

Symptoms of Dysbiosis:

  • Bloating
  • Gas
  • Weight gain
  • Nausea
  • Constipation or diarrhea alternating
  • Rectal itching
  • Fingernails cracked, splitting and weak
  • Acne
  • Undigested food in stool
  • Greasy stool
  • Bruising
  • Fatigue
  • Brain fog
  • Yeast infections vaginal for women
  • Parasite susceptibility

Causes of Dysbiosis: 

  • Medications–laxatives, antibiotics, OCPs
  • Inflammatory diet
    • Sugar, etoh, refined carbs
    • Stress, anxiety
    • Eating foods you know you are allergic to
  • Immunosuppression–stress
  • Hormonal imbalances: thyroid, Perimenopause and menopause

Lab testing/diagnosis:

  • Comprehensive Digestive Stool Analysis / Parasitology (CDSA/P)
    • Stool test
    • Analyze digestion, absorption, blood, pH, bacterial imbalance, yeast and parasites
  • Organix comprehensive profile urine:
    • Functional vitamin and mineral status
    • Amino acid insufficiencies like carnitine and NAC
    • Oxidative damage and antioxidant need
    • Phase I and II detoxification capacity
    • Functional B complex vitamin needs
    • Neurotransmitter metabolites
    • Mitochondrial energy production
    • Methylation sufficiency
    • Lipoic acid and CoQ10 status
    • Markers for bacterial and yeast overgrowth
  • Organix dysbiosis Test:
    • Urine test measuring by-products of microbial metabolism and detecting pathogenic microbial overgrowth


  • Digestin
  • Ortho Digestizyme
  • Aloe (constipation)
  • Magnesium citrate (constipation)
  • Berberine complex
  • A-Biotic 60 gels
  • Biotagen
  • Galactomune
  • Vital-10
  • Thera-Biotic Complete (capsules / powders)