Tag: Carbohydrates

April 11, 2019

Why Salt is So Important on a Ketogenic Diet?

The most common complaint that I get in my office when someone has started a ketogenic diet is, “Doc, I feel fatigued. Will this ever go away?”

That feeling of fatigue, some refer to as the “keto-flu,” is usually due to a couple of things. First, you may not be eating enough fat (I recommend a 1 gram to 1 gram ratio of protein to fat when getting started). Second, you’re not taking in enough salt (specifically sodium, potassium, magnesium and/or zinc). These four salts are essential electrolytes our body requires for proper function.

If salt is the problem, the you will be experiencing leg cramps. Cramps during daytime activity are usually due to low sodium or potassium levels. Cramps that wake you up at night are usually due to low magnesium or zinc. Leg cramps can also be due to hypothyroidism or significant blood sugar swings. Dr. Nally will usually check for this during your visit with him.

“But isn’t too much salt bad for you?” I am frequently asked.

Too much salt is only bad for you if you’re eating a “low-fat” diet.

What if increasing salt intake actually lowered your blood pressure?

Did you know that increasing your salt intake can actually improve your diabetic blood sugar if you are following a correct diet? Could it be that easy?

Almost every patient that I see in the office has a significant worry about salt intake, some greater than others. In fact, some people are so fearful about salt that when I initially began encouraging its use, they told me that I was crazy, and they left my practice.

Has restricting salt over the last 50 years really worked, or is it doing more damage than we think?

That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago. However, his answer never got a mention. In fact, I’ve been in practice for almost 20 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine. Granted, the study is a small sample size of people, only twenty-one. However, the results are profound.

Twenty-one patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day). Glucose tolerance tests were completed with insulin levels at the end of each intervention period.

Insulin Resistance and Hypertension Improve by Adding Salt

Three very noteworthy results happened. First, those patients with insulin resistance and diabetes had improvement in their glucose levels while on 2 grams of sodium supplementation.

Second, those with hypertension also, shockingly, showed improvement in their blood pressure while on the 2 grams of sodium supplementation.

Third, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake. These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”

“But, Dr. Nally, you can’t base your findings on a small group of 21 people,” the experts say.

Yes, it is a small study group. However, these findings are identical to what I, also, see clinically every day in my practice for over 20 years.

We know that the average human needs at a minimum 3 grams of sodium per day and 3 grams of potassium per day. The standard American diet (SAD diet) including processed foods contains 2-3 grams per day of sodium and potassium. In fact, the CDC claims the worst salt containing meals for you are:

Bread
Processed chicken dinners
Pizza
Pasta

Insulin also stimulates additional retention of sodium at the kidney level. If you are insulin resistant, producing excess insulin in response to starches or sugars, you retain notably larger amounts of salt when eating the standard American diet (SAD diet) or a “low-fat” diet. However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt.

Salts, or electrolytes, are essential in normal cellular function. Low salt in the body is like running your car without oil. It will run, but not very efficiently and over the long term will cause problems. This is the cause of the keto-flu I wrote about previously. And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.

How Much Salt Should I Use?

In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle. That’s approximately 1 ½ – 2 teaspoons of salt per day. I like the Redmond’s RealSalt or pink Himalayan salt because these products contains all four types of salt (sodium, potassium, magnesium and zinc).

It is probably that your salt restrictions is making your insulin resistance and blood pressure worse. That’s what the clinical evidences are pointing toward, and it is what I see every day in my office.

Want to know more about a ketogenic life-style? Click the KetoLife link to get some basics.

If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the KetoKart and checking out the products I recommend to jump-start ketosis DocMuscles-style!

Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!

March 11, 2018

Long-Term Weight Loss: Why So Many Fail

Over fifty years of data have demonstrated that creating energy deficit through the reduction in caloric intake is effective in reducing weight. . . However, it is only for the short term (1, 2). The biggest challenge physicians face in the treatment of obesity is that calorie restriction fails when it comes to long-term weight loss.

Isn’t Fasting Effective in Long-Term Weight Loss?

With the craze and popularity of intermittent fasting, some have claimed that intermittent fasting is more effective in weight reduction. Recent results demonstrate that this may also be incorrect. In the short term evaluation of caloric restriction and intermittent fasting, reduction in 15-20 lbs of weight is effectively seen and the highly publicized Biggest Loser’s losing ~ 120 lbs. Intermittent fasting and alternate day fasting have been shown to be more effective in lowering insulin levels and other inflammatory markers in the short term.

There is, however, controversy over maintaining weight loss beyond 12 months in the calorie restriction, intermittent and alternate day fasting groups. Forty different studies in a recent literature review, thirty-one of those studies looking at forms of intermittent fasting, demonstrate that the majority of people regain the weight within the first 12 months of attempting to maintain weight loss(3, 5). This is, also, what I have seen for over 18 years of medical practice.

Is Calorie Restriction the Only Way to Lose Fat?

Numerous “experts” claim that the only way to reduce fat is “caloric deficit.” Variations through the use of intermittent, long-term or alternate day fasts can be found all over the internet. In regards to calorie restriction, these “experts” with nothing more than a personal experience and a blog to back their claims preach this louder than the “televangelists” preach religion. Based on the faith that many place in this dogma, it could be a religion. What causes belief in this dogma is that weight and fat loss actually does occur with caloric restriction to a point. The average person will lose 20-25 lbs, however, within 12 months of achieving this goal, most people regain all the weight. (No one ever mentions the almost universal problem with long-term weight loss, especially those “experts.”)

Prolonged calorie restricted fasts, intermittent fasts, and alternate day fasts are often grouped together into the fasting approach, causing significant confusion among those that I speak to and counsel in my office. There is great data that alternate day fasts do not have the reduction in resting energy expenditure that prolonged fasting, intermittent fasting and calorie restriction cause. However, none of these approaches appears to solve the problem of weight re-gain after long-term (12-24 months into maintenance) weight loss (3). And, a recent study of 100 men participating in alternate day fasting showed that there was a 38% dropout rate, implying that without close supervision and direction, maintenance of this lifestyle is not feasible for over 1/3rd of those attempting it.

Long-Term Weight Loss Failure Brings Tears

Failure on calorie restricted diets, low fat diets, and intermittent fasting diets with weight regain at twelve to twenty-four months is the most common reason people end up in my office in tears. They’ve fasted, starved themselves, calorie restricted, tried every form of exercise, and still regained the weight. Trainers, coaches and “experts” have belittled them for “cheating” or just not keeping to the diet. Yet, we know that calorie restriction and intermittent fasting cause a rebound in leptin, amilyn, peptid YY, cholecystikinin, insulin, ghrelin, gastric inhibitory peptide and pancreatic poly peptide by twelve months causing ineffective long-term weight loss (6). The dramatic rise in these hormones stimulates tremendous hunger, especially from ghrelin and leptin.

N Eng J Med 27 Oct 2011. Mean (±SE) Fasting and Postprandial Levels of Ghrelin, Peptide YY, Amylin, and Cholecystokinin (CCK) at Baseline, 10 Weeks, and 62 Weeks.

Although less problematic in alternate day fasting, these calorie restricted approaches also cause dramatic slowing of the metabolism at the twelve month mark. In many cases, the metabolic rate never actually returns to baseline, creating even more difficulty in losing further weight or even maintaining weight (6).

N Engl J Med 27 Oct 2011. Mean changes is weight from 0 – 62 weeks.

Is Gastric Bypass or Gastric Sleeve the Solution?

Gastric bypass and the gastric sleeve procedures have been touted as the solution to this problem, as they decrease ghrelin, however, 5-10 years later, these patients are also back in my office. They find that 5-10 years after these procedures the weight returns, cholesterol and blood pressure rise, and diabetes returns. These hormones kick into high gear, stimulating hunger in the face of a slowed metabolism, that to date, has been the driver for weight regain in the majority of people. People find it nearly impossible to overcome the hunger. You may have experienced this, I know I have.

It’s the Hormones, Baby!

So, what is the answer? It’s the hormones. (WARNING – You’ll hear that when your wife is pregnant, too, gentlemen). We are hormonal beings, both in weight gain, and in pregnancy. Trying to preach calorie control to a hormonal being is like showing up at the brothel to baptize the staff. You might get them into the water, but you’re probably not getting them returning weekly to church or pay a tithe.

So, how do you manipulate the hormones in a way to control the rebounding hunger and suppression of metabolism? This is where we put a bit of twist on the knowledge we’ve gained from alternate day fasting. Recent research shows that “mild” energy deficit in a pulsatile manner, that has the ability to mimicking the body’s normal bio-rhythm’s is dramatically effective in reducing weight and maintaining normal hormonal function without cause of rebound metabolic slowing (4).

Pulsed Mild Energy Restriction

What does this mean in layman’s terms? It means that if we provide a diet that maintains satiety hormones while providing a period of baseline total energy expenditure needs and a period of mildly reduce caloric intake in a pulsed or cyclic manner, greater weight loss occurs and there is no rebound of weight 1-2 years later.

The main reason I’ve not jumped on the intermittent fasting band wagon is the shift in leptin, amylin, ghrelin and GLP-1 signaling that regularly occurs at the 6-12 month mark. The rebound of these hormones causes weight re-gain and is what prevents successful long-term weight loss. A number of people come to my office and tell me they couldn’t follow a ketogenic diet, so they’re doing intermittent fasting and it works . . . for a while. Then, they end up in my office having hit a plateau or fallen off the wagon and regained all the weight. They are completely confused and don’t understand what happned. Most of them are convinced it’s their thyroid or cortisol and they’ve seen every naturopath and functional medicine doctor in town.

What people really need is a simple approach to long-term weight loss without having to spend the night in the physiology lab every two weeks sleeping under a ventilated hood system.

The Ketogenic Lifestyle is a Pulsed Energy Lifestyle

First, it is essential to turn off the insulin load. Insulin is the master hormone. This is done by a ketogenic lifestyle that restricts carbohydrates.
Second, providing adequate protein to supply maintenance of muscle and testosterone is key.
Third, providing adequate fat is the simple way to maintain leptin, ghrelin, amylin, GLP-1 (among the others) and long-term weight loss. Can you eat too much fat? Of course you can. But, because each of us have differing levels of stress and activity each day, this fat intake becomes the lever for hunger control.
Fourth, the use of exogenous ketones ensures easily accessible ketone (short chain fatty acids) to modulate adipose (white fat) signaling of the liver without large caloric intake through the portal vein by first pass of liver metabolism. The ketones also help stabilize the gut bacteria. The combination of hormone balance between the liver and fat cells and improvement of gut bacteria suppresses key hunger hormones and aids glucose regulation between the fatty tissues and the liver. Ketones, both endogenous and exogenous, suppress production of TNF-alpha, IL-6, resistin, and stabilize production of adiponectin and leptin from the adipose cells (7, 8, 9).

In my office, once we calculate the basic protein needs daily, we start with a 1:1 ratio of protein to fat. Then, the fat is adjusted up or down based on hunger. Remember, hunger occurs, because your body produces hormones. The addition of fat to a diet that is not stimulating large amounts of insulin resets the hormone patterns back to normal without causing weight gain.

Give Obese People Fat Ad Libitum?

“Sure, Dr. Nally, but what about those people who don’t know if they are hungry, bored, stressed or just have a bacon fixation? You can’t just give them all the fat they want?!”

Why not? Implying that people aren’t smart enough to know when they are full is a bit of a fascist philosophy, don’t you think?

Do people over eat? Sure they do. But, I’ve found that when you give people an antidote to hunger (using fat intake in the presence of stabilized insulin levels) over a few months, people begin to recognize true hunger from other forms of cravings. This is especially true when they keep a diet journal. This gives people the ability to begin listening to their own bodies, responding accordingly and governing their stress, eating, exercise and activity. Keeping a diet journal is key to long-term weight loss. And, isn’t helping people use their own agency to improve their health really what we’re trying to do?

Interestingly, doing this over the years seems to line up with the findings of this year’s MATADOR study in the International Journal of Obesity. They found that mild intermittent energy restriction of about 30-33% for two weeks, then interrupting this with two weeks of a diet that was energy balanced for needs improved both short and long-term weight loss efficiency (4). In looking at my, and my patient’s diet journals, this energy restriction of about 1/3 of needed calories cyclically seems to happens naturally with a ketogenic lifestyle, without even counting calories. (Calories are a swear-word in my office).

What does the correct long-term wight loss program look like in a diet or meal plan? Well, you’ll have to join the Ketogenic Lifestyle 101 Course to see what that really means to you individually. I look forward to seeing you there.

Want to find out more about the Ketogenic Lifestyle 101 course? CLICK HERE.

Have you read my book The Keto Cure? Get a signed copy from me by clicking HERE.

References:

Bronson FH, Marsteller FA. “Effect of short-term food deprivation on reproduction in female mice.” Biol Reprod. Oct 1985; 33(3): 660-7. https://www.ncbi.nlm.nih.gov/pubmed/4052528?dopt=Abstract&holding=npg
Connors JM, DeVito WJ, Hedge GA. “Effects of food deprivation on the feedback regulation of the hypothalamic-pituitary-thyroid axis of the rat.” Endocrinology. Sep 1985. 117(3): 900-6. https://www.ncbi.nlm.nih.gov/pubmed/3926471?dopt=Abstract&holding=npg
Seimon RV, Roekenes JA, Zibellini J, Zhu B, Gibson AA, Hills AP, Wood RE, King NA, Byrne NM, Sainsbury A. “Do intermittent diets provide physiological beneftis over continuous diets for weight loss? A systematic review of clinical trials.” Mol Cell Endo. 15 Dec 2015. 418(2): 153-172. https://www.sciencedirect.com/science/article/pii/S0303720715300800
Byrne NM, Sainsbury A, King NA, Hills AP, Wood RE. “Intermittent energy restriction improves weight loss efficiency in obese men: the MATADOR study.” Int J Obes. 2018. 42:129-138. https://www.nature.com/articles/ijo2017206
Trepanowski JF, Kroeger CM, Barnosky A. “Effect of Alternate-Day Fasting on Weight Loss, Weight Maintenance, and Cardioprotection Among Metabolically Healthy Obese Adults.” JAMA Intern Med. Jul 2017. 177(7): 930-938. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2623528?redirect=true
Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, Proietto J. “Long-term persistence of hormonal adaptations to weight loss.” N Engl J Med. 27 Oct 2011. 365: 1597-1604. http://www.nejm.org/doi/full/10.1056/NEJMoa1105816
Asrih M et al., “Ketogenic diet impairs FGF21 signaling and promotes differential inflammatory responses in the liver and white adipose tissue.” PlosOne. 14 May 2015. Open Access. https://doi.org/10.1371/journal.pone.0126364
Veniant MM et al. “FGF21 promotes metabolic homeostasis via white adipose and leptin in mice.” PlosOne. Jul 2012. Open access. https://doi.org/10.1371/journal.pone.0040164
Whittle AJ, “FGF21 conducts a metabolic orchestra and fat is a key player.” Endocrinology. 1 May 2016. 157(5): 1722-1724.

January 13, 2017

You're Doing It Wrong: Can 50 Years of Nutritional Advise Really be that Wrong?

Listen in as Dr. Nally discusses how we got to be the fattest and sickest country in the world after 50-60 years of bad science influenced by the media and politics. How can a ketogenic diet help the diseases of civilization? Listen in and then click the link in the menu above to get my six-part mini course instruction.

We also discuss Dr Nally’s daily diet and his use of exogenous ketones.

January 31, 2016

Ketogenic Lifestyle Rule #2: Life Begins at the Edge of Your Comfort Zone

We have been taught for over 50 years that the minimum carbohydrate intake necessary to maintain health is 130 grams per day, with the average diet of 2000 calories per day containing around 300 grams per day based on 1977 recommendations that 55-60% of are dietary intake should come from carbohydrates. This value was initially established during World War II by a committee of scientists tasked with determining dietary changes that might effect national defense (1). These “guidelines,” originally called the Recommended Daily Allowances (RDA) and accepted by many as the gospel truth, have been modified every ten years and in 1997 changed to the Dietary Reference Intake (DRI). However, the recommended carbohydrate values have not changed other than “avoiding added sugars” in the most recent 2015 recommendations.

In light of the fact that there are NO actual diseases caused by lack of carbohydrate intake, most dietitians and physicians still preach the carbohydrate dogma originally outlined by the RDA. I say dogma, because these recommendations are based on a diet that vilifies fat, particularly animal fat like red meat. Say the words “red meat” around a dietician these days you’d think Voldemort (“He Who Shall Not Be Named”) had returned.

I bring up the carbohydrate quandary because it is a question that I am asked every single day. The question that seems to be asked of me, more and more, is what exactly is a carbohydrate?

Let’s make it simple. There are really only three types of carbohydrates:

Sugar
Starch (known as complex carbohydrates)
Fiber

Let’s start with Sugar. The simple form of carbohydrates, and the form that spikes your blood sugar and insulin rapidly, are called mono-saccharides (glucose, galactose, fructose & xylose). When two of these mono-saccharides are bound together they form disaccharides like sucrose, also known as “table sugar” (glucose + fructose), lactose found in milk (glucose + galactose), and maltose found in cereals and sweet potatoes (glucose + glucose).

Milk Sugar or Lactose (glucose + glucose)

The simple monosaccharides or disaccharides are easy broken into their mono-saccharide form in the blood stream and require the body to produce insulin to be used. The person with insulin resistance, impaired fasting glucose or type II diabetes often produces 2-10 times the normal amount of insulin to correctly use these mono-saccharides (see why this is a problem in: The Dreaded Seven: Seven Detrimental Things Caused By High Insulin Levels). Remember, fruit is also simple sugar containing the mono-saccharide fructose . . . which we call “natures candy” in my office.

“Yea, I know sugar is bad for me, but Dr. Nally, I just eat the good starches.”

If I had a nickel for every time I’ve herd that phrase . . .

We’ve become comfortable with shunning fat and “simple sugar,” but in the process we’ve been eating more “good starch.” But the “good starches” are also saccharides – just in longer chains of more than three glucose molecules bound together. Our gut easily breaks the bonds between the glucose links and turns these starches into mono-saccharides to be used as fuel. It takes a bit longer than the simple sugars above, so the release of insulin is slower (which is why it has a better glycemic index score), but whether you produce the insulin in the first hour or the second hour after eating it, insulin is still insulin. In the case of insulin resistance, the damage is still done.

These good starches make up “comfort food” like bread, rice, pasta, potatoes, corn, grains & oats. To the patient with insulin resistance, impaired fasting glucose or type II diabetes, the higher insulin response stimulates increased weight gain, rise in cholesterol, shift in hormone function and progression of atherosclerosis (vascular and heart disease). See the recent article on Why Your Oatmeal is Killing Your Libedo.

What about “resistance starches?” These are still starches and I am finding clinically that they still cause a rise in insulin and push people out of ketosis (See Common Ketosis Killers).

Finally, Fiber. Fiber is a carbohydrate, however, it is the indigestible part of the plant. Fiber has double bonds between the saccharides that human gastrointestinal tracts cannot digest. In most cases, fiber passes right through the intestines without being digested. It actually acts like a broom for your colon, helping the intestines to move nutrients through the system. This is why I recommend 1-2 leafy green salads a day for most patient’s following ketogenic diet. Fiber does help to promote bowel function.

The Leafy Greens

Fruit, non-green vegetables, pasta, grains and breads do contain good sources of fiber, however, these foods also have absorbable starches making them problematic as noted above.

The take home message is this, the use of starch or simple carbohydrate will be problematic for weight loss, cholesterol control, blood sugar control or blood pressure control in a patient with insulin resistance.

Therefore, the ketogenic lifestyle truly begins at the end of your comfort zone.

November 25, 2015

Adrenal Insufficiency, Adrenal Fatigue, PseudoCushing’s Syndrome – Oh My!

Adrenal Fatigue? Adrenal Insufficiency? Cortisol? PseudoCushing’s Syndrome? What do these terms mean and why are they all over the internet these days? And, what do they have to do with your weight loss?

This was our topic this evening on PeriScope. Katch Dr. Nally speak about this topic with rolling comments at Katch.me/docmuscles. Or you can watch the video below:

If you’re not sure about what this is, you’re not alone. I think I’ve heard the term “Adrenal Fatigue” at lease four times a day for the last three months. If you ask your doctor, they’ll probably scratch their heads too. The funny thing is that “Adrenal Fatigue” isn’t a real diagnosis, but it is all over the internet and it shows up in the titles of magazines in the grocery store every day. There’s even and “Adrenal Fatigue For Dummies” so it must be real, right?!

No. It isn’t a real diagnosis. It is a conglomeration of symptoms including fatigue, difficulty getting out of bed in the morning, and “brain fog” that have been lumped together to sell an “adrenal supplement.” (Sorry, but that’s really what it is all about.) Do a Google search and the first five or six sites describing adrenal fatigue claim the solution is taking their “special adrenal supplement.”

I know what you’re thinking, “Your just a main stream, Western Medicine doctor, Dr. Nally, you wouldn’t understand.” Actually, I do understand.

Adrenal fatigue has risen in popularity as a “lay diagnosis” because many patients show up at their doctors office with significant symptoms that actually interfere with their ability to function, and after all the testing comes back negative for any significant illness, they are told that they are normal. But the patient still has the symptoms and no answer or treatment has been offered. It’s discouraging. . . very discouraging.

That’s because the symptoms are actually the body’s response to chronic long term stress. Many of my patients, myself included, have found themselves “stuck” in their weight loss progression, feeling fatigued, struggling to face the day, with a number of symptoms including cold intolerance, memory decline, difficulty concentrating, depression, anxiety, dry skin, hair loss, and even infertility in some cases. Is it poor functioning adrenal glands? No, your feeling this way because the adrenal glands are actually doing their job!!

If the adrenal glands weren’t working you’d experience darkening of the skin, weight loss, gastric distress, significant weakness, anorexia, low blood pressure, and low blood sugar. The symptoms are actually called Addison’s disease and it is actually fairly rare (1 in 100,000 chance to be exact). So what is causing the symptoms you ask?

There are a number of reasons, but one that I am seeing more and more frequently is “Pseudo-Cushings’s Syndrome.” Pseudo-Cushing’s Syndrome is a physiologic hypercortisolism (over production of cortisol) that can be caused by five common issues:

Chronic Physical Stress
Severe Bacterial or Fungal Infections that Go Untreated
Malnutrition or Intense Chronic Exercise
Psychological Stress – including untreated or under-treated depression, anxiety, post-traumatic stress, or dysthymia (chronic melancholy)
Alcoholism

The psychiatric literature suggest that up to 80% of people with depressive disorders have increased cortisol secretion (1,2,3). People with significant stressors in their life have been show to have an increased corsiol secretion. Chronic stress induces hyperactivity of the hypothalamic-pituitary-adrenal axis causing a daily, cyclic over production of cortisol and then normalization of cortisol after resolution of the stressor. This cortisol response is not high enough to lead to a true Cushing’s Syndrome, but has the effect of the symptoms listed above and begins with limiting ones ability to loose weight.

I’m convinced that this is becoming more and more prevalent due to the high paced, high-stress, always on, plugged in, 24 hour information overload lives we live.

What is cortisol? It is a steroid hormone made naturally in the body by the adrenal cortex (outer portion of the adrenal gland). Cortisol is normally stimulated by a number of daily activities including fasting, awakening from sleep, exercise, and normal stresses upon the body. Cortisol release into the blood stream is highest in the morning, helping to wake us up, and tapers into the afternoon. Cortisol plays a very important role in helping our bodies to regulate the correct type (carbohydrate, fat, or protein) and amount of fuel to meet the bodies physiologic demands that are placed upon it at a given time (4,5,6).

Under a stress response, cortisol turns on gluconeogensis in the liver (the conversion of amino acids or proteins into glucose) for fuel. Cortisol, also, shifts the storage of fats into the deeper abdominal tissues (by stimulating insulin production) and turns on the maturation process of adipocytes (it makes your fat cells age – nothing like having old fat cells, right?!) In the process, cortisol suppresses the immune system through an inhibitory effect designed to decrease inflammation during times of stress (7,8,9). If this was only occurring once in a while, this cascade of hormones acts as an important process. However, when cortisol production is chronically turned up, it leads to abnormal deposition of fat (weight gain), increased risk of infection, impotence, abnormal blood sugars, brain fog, head
aches, hypertension, depression, anxiety, hair loss, dry skin and ankle edema, to name a few.

The chronic elevation in cortisol directly stimulates increased insulin formation by increasing the production of glucose in the body, and cortisol actually blunts or block-aids the thyroid function axis. Both of these actions halt the ability to loose weight, and drive weight gain.
Cortisol also increases appetite (10). That’s why many people get significant food cravings when they are under stress (“stress eaters”). Cortisol also indirectly affects the other neuro-hormones of the brain including CRH (corticotrophin releasing hormone), leptin, and neuropeptide Y (NPY). High levels of NPY and CRH and reduced levels of leptin have also been shown to stimulate appetite and cause weight gain (10-11).

How do you test for Pseudo-Cushing’s Syndrome?

Testing can be done by your doctor with a simple morning blood test for cortisol. If your cortisol is found to be elevated, it needs to be repeated with an additional 24 hour urine cortisol measurement to confirm the diagnosis. If Cushing’s Syndrome is suspected, some additional blood testing and diagnostic imaging will be necessary. Pseudo-Cushing syndrome will demonstrate a slightly elevated morning cortisol that doesn’t meet the criteria for true Cushing’s type syndrome or disease.

How do you treat it?

First, the stressor must be identified and removed. Are you getting enough sleep? Is there an underlying infection? Is there untreated anxiety or depression present? Are you over-exercising? These things must be addressed.

Second, underlying depression or anxiety can be treated with counseling, a variety of weight neutral anti-depressant medications or a combination of both. Many of my patients find that meditation, prayer, and journaling are tremendous helps to overcoming much of the anxiety and depression they experience.

Third, adequate sleep is essential. Remove the television, computer, cell phone, iPad or other electronic distraction from the bedroom. Go to bed at the same time and get up at the same time each day. Give yourself time each day away from being plugged in, logged in or on-line.

Fourth, mild intensity (40% of your maximal exertion level) exercise 2-3 days a week was found to lower cortisol; however, moderate intensity (60% of your maximal exertion level) to high intensity (80% of your maximal exertion level) exercise was found to raise it (12). A simple 20 minute walk, 2-3 times per week is very effective. Find a hobby that you enjoy and participate in it once or twice a week. Preferably, a hobby that requires some physical activity. The activity will actually help the sleep wake cycles to improve.

Fifth, follow a low carbohydrate or ketogenic diet. Ketogenic diets decrease insulin and reverse the effect of long term cortisol production. Ketogenic diets a have also been shown to decrease or mitigate inflammation by reducing hyperinsulinemia commonly present in these patients (13).

So, the take home message is . . . take your adrenal glands off of overdrive.

References:

Pfohl B, Sherman B, Schlechte J, Winokur G. Differences in plasma ACTH and cortisol between depressed patients and normal controls. Biol Psychiatry 1985; 20:1055.
Pfohl B, Sherman B, Schlechte J, Stone R. Pituitary-adrenal axis rhythm disturbances in psychiatric depression. Arch Gen Psychiatry 1985; 42:897.
Gold PW, Loriaux DL, Roy A, et al. Responses to corticotropin-releasing hormone in the hypercortisolism of depression and Cushing’s disease. Pathophysiologic and diagnostic implications. N Engl J Med 1986; 314:1329.
Ely, D.L. Organization of cardiovascular and neurohumoral responses to stress: implications for health and disease. Annals of the New York Academy of Sciences (Reprinted from Stress) 771:594-608, 1995.
McEwen, B.S. The brain as a target of endocrine hormones. In Neuroendocrinology. Krieger and Hughs, Eds.: 33-42. Sinauer Association, Inc., Massachusetts, 1980.
Vicennati, V., L. Ceroni, L. Gagliardi, et al. Response of the hypothalamic- pituitary-adrenocortical axis to high-protein/fat and high carbohydrate meals in women with different obesity phenotypes. The Journal of Clinical Endocrinology and Metabolism 87(8) 3984-3988, 2002.
Wallerius, S., R. Rosmond, T. Ljung, et al. Rise in morning saliva cortisol is associated with abdominal obesity in men: a preliminary report. Journal of Endocrinology Investigation 26: 616-619, 2003.
Epel, E.S., B. McEwen, T. Seeman, et al. Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat.
Psychosomatic Medicine 62:623-632, 2000.
Tomlinson, J.W. & P.M. Stewart. The functional consequences of 11_- hydroxysteroid dehydrogenase expression in adipose tissue. Hormone and Metabolism Research 34: 746-751, 2002.
Epel, E., R. Lapidus, B. McEwen, et al. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior.Psychoneuroendocrinology 26: 37-49, 2001.
Cavagnini, F., M. Croci, P. Putignano, et al. Glucocorticoids and neuroendocrine function. International Journal of Obesity 24: S77-S79, 2000.
Hill EE, Zack E, Battaglini C, Viru M, Vuru A, Hackney AC. Exercise and circulating cortisol levels: the intensity threshold effect. J Endocrinol Invest. 2008. Jul;31(7):587-91.
Fishel MA et al., Hyperinsulinemia Provokes Synchronous Increases in Central Inflammation and β-Amyloid in Normal Adults. Arch Neurol. 2005;62(10):1539-1544. doi:10.1001/archneur.62.10.noc50112.

October 1, 2015

Fructose and High Triglycerides Lead to Leptin Resistance

I can’t help myself. Some days I enjoy a good murder mystery, but on others, I enjoy a good journal article elucidating our understanding of leptin. No, leptin is not a tiny Irish folk character or even a superhero. Leptin is a hormone. It’s made by fat cells. Anything made by fat cells becomes fascinating to a “fat doctor.”

Why is learning about leptin illuminating?

Well, if Sir Arthur Conan Doyle was an Obesity Specialist, the mystery would have been that Mr. Plump was killed by the wrench in the kitchen, but the wrench seems to have never left tool case in the garage. No one has been able to figure out how leptin, the allegorical wrench, plays its roll in lepin resistance. We know that a lack of leptin allows hunger to persist and a person without leptin will continue to eat without the sensation of feeling full – leading to obesity. What we haven’t understood is – what causes the brain to no longer sense larger and larger amounts of leptin being produced by those who are obese.

That is . . . we haven’t understood it until now. . .

We have known for some time that the hormone leptin is a key hormone produced by the adipose (fat) cells that suppresses hunger. A majority of obese patients in my clinic have elevated circulating leptin levels 2-10 times the normal levels. We know that a lack of leptin leads to obesity, but the patients that I see in the office are producing an over abundance consistent with leptin resistance. The leptin signal is not being recognized by the brain. This is very similar to type II diabetes and insulin resistance. The pancreas is producing an over abundance of insulin, but the cells are recognizing the signal to let the glucose in through the door way.

Three recent and very interesting studies have pointed to the probable cause. First, one of the most common genetic disorders causing human obesity is loss of function of the melanocortin receptor.

Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

If the MC-4R receptor is broken, suppression of appetite is limited, continued eating occurs and weight gain continues. Leptin, produced by every adipose cell in the body, is carried in the blood stream to the brain and must pass through the blood-brain barrier. Once it crosses the blood-brain barrier and enters the hypothalamus, it has a stimulatory effect on the MC-3R receptor in the Arcuate Nucleus of the hypothalamus causing stimulation of the MC-4R receptor in the Parventricular Nucleus and Lateral Hypothalamus to turn off hunger.

Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

However, if leptin cannot cross the blood brain barrier, the signal is never received from the adipose cells and continued eating without satiation (feeling full) persists. Studies have shown that dietary fructose ingestion alone or in combination with diets high in fat suppress the transmission of leptin across the blood-brain barrier.

Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

Fructose is the primary component of high-fructose corn syrup, and makes up 45-50% of every other type of natural form of sugar (sucrose). Yes, it’s the major component found in table sugar, brown sugar, honey, agave, molasses and maple syrup. This is why a Paleolithic Diet isn’t fully effective for people with leptin resistance.

Lastly, anything that raises triglycerides inhibits leptin from crossing the blood-brain barrier.

Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

Insulin has a direct effect on triglycerides. (See the articles “Insulin Resistance & The Horse,” “Fat Thoughts on Cholesterol,” “Ketogenic Living” and “So, What is this Ketogenic Thing?“). If your insulin levels go up, triglyceride production goes up. The patient with insulin resistance, pre-diabetes, impaired fasting glucose or type II diabetes produces between two to ten times the normal amount of insulin when eating the standard American diet (SAD diet). These patients have significant triglyceride elevation because of the high insulin response to carbohydrates in their diet. (Many of them were told by their doctor that “It’s just genetic so take your Lipitor.”) Statin drugs lower the LDL-C (calculated “bad cholesterol” level), but don’t reduce triglycerides effectively. Inadequate treatment of high triglycerides allows poor blood-brain barrier transmission of leptin and worsening leptin resistance.

In fact, this is the challenge and problem with the “frequent fasting” or “intermittent fasting” fad for weight loss that has been popping up in the blogosphere. If fasting reaches a state of starvation (which is a very fine line metabolically), it stimulates a stress response . . . causing a spike in cortisol, release of glycogen (a form of sugar), a compensatory release of insulin and a spike in triglycerides. If you have tried intermittent fasting and you’ve gained weight, you are probably not “fasting,” your probably “starving.” We’ve known for years that triglycerides are elevated in starvation. This diminishes leptin’s ability to cross the blood-brain barrier and leads to worsening leptin and insulin resistance.

High leptin levels caused by leptin resistance also seems to play a significant role in the development of diabetic retinopathy – damage to the tiny blood vessels at the back of the eye feeding the retina. Diabetic retinopathy starts insidiously without any symptoms initially and can lead to eventual blindness if not treated. Leptin seems to upregulate vascular endothelial growth factor (VEGF) which leads to narrowing of the blood vessels called “ischemia.” Chronic ischemia of the retinal vessels leads to damage to the delicate retinal cells of the eye.

So what do you do if you have leptin resistance. First, eliminate carbohydrates from your diet, especially sugars, high fructose corn syrup and any other form of simple sugar. This is why I am such a big fan of low carbohydrate, high fat diets.

Second, lower your triglycerides. This is done through decreasing overall insulin loads and is very effectively accomplished with a ketogenic diet. You can find this in my book, The KetoCure. Some additional great sources are KetoClarity, The Art and Science of Low Carbohydrate Living, and The Ketogenic Cookbook.

Third, use a supplement containing alpha-lipoic acid, carnosine high gamma vitamin E and benfothiamin (derivative of Vitamin B1). These have been demonstrated to decrease inflammation and render protection to the blood vessels.

The use of Epigallocatechin gallate (EGCg), a derivative extract of green tea, has been shown to repress hepatic glucose production, one of the insidious factors of insulin resistance, and may play a role in stabilizing the effect insulin has on production of triglycerides. You should consider using KetoEssentials. It is my specially formulated multivitamin that contains all of the above supplements, and includes methylated folic acid (B9), the necessary vitamin B6 & B12, chromium, vandium & zinc that help to further stabilize insulin resistance.

Fourth, get a good night’s sleep. Lack of sleep causes a stress response, increases cortisol, raises blood sugar and insulin leading to further leptin resistance.

Fifth, mild to moderate resistance exercise has been shown for years to improve insulin resistance significantly. If you’re not exercising, take a 20 minute walk 2-3 times per week, ride a bike for 20 minutes, start a weight lifting program, consider yoga or Pilates, Remember, jumping to conclusions, flying off the handle, carrying things too far, dodging responsibility and pushing your luck don’t qualify as resistance exercise.

Above all, if you’re having trouble losing weight, controlling insulin or leptin, see your doctor. He or she can really help.

References:

Ray F. Gariano, Anjali K. Nath, Donald J. D’Amico, Thomas Lee, and M. Rocio Sierra–Honigmann. “Elevation of Vitreous Leptin in Diabetic Retinopathy and Retinal Detachment.” Invest Ophthalmol Vis Sci. 2000;41:3576–3581
Hammes HP, Du X . “Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.” Nat Med. 2003 Mar;9(3):294-9. Epub 2003 Feb 18.
Hipkiss AR, Brownson . “Reaction of carnosine with aged proteins: another protective process?” Ann N Y Acad Sci. 2002 Apr;959:285-94.
Zachary A. Knight, K. Schot Hannan, Matthew L. Greenberg, Jeffrey M. Friedman. “Hyperleptinemia Is Required for the Development of Leptin Resistance.” PLoS ONE 5(6): e11376. doi:10.1371/journal.pone.0011376.
Min-Diane Li. “Leptin and Beyond: An Odyssey to the Central Control of Body Weight.” The Yale Journal of Biology and Medicine. 2011;84(1):1-7.
Eri Suganami, Hitoshi Takagi,Hirokazu Ohashi, Kiyoshi Suzuma, Izumi Suzuma, Hideyasu Oh, Daisuke Watanabe, Tomonari Ojimi, Takayoshi Suganami, Yasushi Fujio, Kazuwa Nakao, Yoshihiro Ogawa and Nagahisa Yoshimura. “Leptin Stimulates Ischemia-Induced Retinal Neovascularization: Possible Role of Vascular Endothelial Growth Factor Expressed in Retinal Endothelial Cells.” Diabetes. September, 2004. vol. 53 no. 9 2443-2448
Joseph R. Vasselli, Philip J. Scarpace, Ruth B. S. Harris, and William A. Banks. “Dietary Components in the Development of Leptin Resistance.” Adv. Nutr. 2013: 4: 164–175.
Joseph R. Vasselli. “Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance.” Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1365-9. doi: 10.1152/ajpregu.90674.2008. Epub 2008 Sep 10.
Waltner-Law ME, Wang XL Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem. 2002 Sep 20;277(38):34933-40. Epub 2002 Jul 12.

April 17, 2015

Why Your Oatmeal is Killing Your Libido

Have you noticed that there are a large number of advertisements in the media about checking your testosterone or “Low T” Syndrome? It seems like this is the new advertising trend on the radio and late night TV.

Suddenly, everyone’s testosterone is low and men are complaining about their libido, . . . or are they?

Benefits of Testosterone Optimization. (Image Credit: ArtOfManliness.com)

If you practice medicine long enough, you’ll see a trend that seems to have arisen as our waistlines have expanded. About half of the men in my office with insulin resistance, pre-diabetes or diabetes have low testosterone levels. But this shouldn’t be a surprise. Type II diabetes, metabolic syndrome and insulin resistance are all driven by an over production in insulin in response to a carbohydrate load in the meal. Patients with these conditions produce between two to ten times the normal insulin in response to a starchy meal. A number of studies both in animal and human models demonstrate that insulin has a direct correlation on testosterone suppression in the blood. This has been demonstrated in both men and women. In fact, glucose intake has been shown to suppress testosterone and LH in healthy men by suppressing the gonadal hormone axis and more predominant testosterone suppression is seen in patient with insulin resistance or metabolic syndrome.

Image Credit: www.townsendletter.com/July2012/metsyndrome0712.html

In fact, to put it simply, insulin increases the conversion (aromitization) of testosterone to estrogen in men (it does the opposite in women). Interestingly, Leptin resistance has a similar effect. I tend to see the worst lowering of testosterone in men with both insulin and leptin resistance.

How to you improve your testosterone? Supplemental testosterone has been shown to help, but it comes with some risks, including prostate enlargement and stimulating growth of prostate cancer. The most natural way to improve your testosterone is to change your diet.

A low carbohydrate or ketogenic diet turns down the insulin production and allows the testosterone to be available for use by the body. A ketogenic diet has the effect of reducing leptin resistance as well through weight loss. A simple dietary change of this type is frequently seen in my office to increase testosterone by 100-150 points.

KetoOS – Drinkable Exogenous Ketones

What is a ketogenic diet? It is a diet that restricts carbohydrates to less than 50 grams per day, thereby causing the body to use ketones as the primary fuel source. So, for breakfast tomorrow morning, hold the oatmeal (1/2 cup of Quaker Instant Oatmeal is 31 grams of carbohydrates) and have the bacon and eggs. And, rather than have the cheesecake for desert this evening, have an extra slice of steak butter on your rib-eye and hold the potato.