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Low Sodium Diets Don’t Have to be Bland…

In Uncategorized on November 2, 2013 at 11:32 pm

I remember a particular year when I visited my grandparents’ home in Texas. I must have been 10 years of age or so.  Anyone who knew them would readily agree that they were the epitome of kindness. Each time I visited, I anticipated yummy food, an ancient video game set, and classic movies like Chitty Chitty Bang Bang. Everything in that visit went as usual except for one thing: the food. The usually tasty, homemade food  now was noticeably bland.

I overheard my parents chatting about how there was no salt in the food–I wasn’t the only one who noticed. Learning that the “blandness” was due to a lack of salt, I quickly inquired about this paucity of table salt. Come to find out, there was no shortage of salt at the grocery store; my grandmother had purposely excluded the salt from her recipes  to help my grandfather with his heart problems. The food tasted much better after my mother retrieved a salt shaker from the kitchen cabinet.

Twenty years later, I was no longer sampling salt-less food; rather, I was learning about it in medical school.  Come to find out, dietary sodium reduction was a legitimate lifestyle modification recommended by the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. I could more than accurately conclude that my late grandfather had high blood pressure. The JNC 7 reports that blood pressure can drop by 2-8mmHg with reduction in dietary sodium. In Naturopathic Medicine we learned that appropriate sodium substitutes could make sodium reduction more achievable without compromising the taste of food. Other salts exist that contain other substances than sodium.

Despite the evidence behind low sodium diets, I asked myself: How does sodium affect blood pressure? I would discover that answer much later while teaching kidney physiology as an adjunct professor. The overall answer is a complex one; yet, it can be explained simply: Sodium(normal table salt consists of Sodium and Chloride) increases your blood osmolarity which ultimately lead to an increase in blood volume.

Physicians employ a number of medications to decrease blood volumes in patients with high blood pressure including diuretic medications. Lower blood volumes ultimately leads to lower blood pressures. Our body’s natural responce to an increased sodium ingestion is to drink more water and to reabsorb more water from the urine in the kidneys, ultimately leading to higher blood volumes and higher blood pressure. Our body is trying to dilute a sodium concentrated blood stream by filling it with more water by using  a force commonly known as osmosis in the kidneys and by making us drink more.

So don’t fret. If a low-sodium diet has been recommended to you, there is still hope of a tasty meal with sodium-free salts.

 

Relax & Eat Your Cheesburgers!

In Uncategorized on September 26, 2013 at 3:20 pm

I was in my first year of medical school when Dr. Lichtenstein shared an anecdote with us about one of his clients. The patient was an obese salesman who had problems with his digestive tract. He was always on the road and described having to squeeze “into stalls at gas stations or fast food restaurants, believing he had to dodge glaring looks of disapproval each time.”[1]  He had a number of other complaints that he did not want to address. He wanted to have one bowel movement a day before work– that was it. At first, Dr. Lichtenstein didn’t know what to do because the man did not want to change his diet, lose weight, take any supplements, or begin any exercise.

Dr. Lichtenstein describes that the success he had with this patient had to do with teaching the man about how the digestive tract works, and then telling him to simply to park his car at meal time and quietly eat his meals at scenic overlooks.

The principle Dr. Lichtenstein was using in his prescription had to do with how the parasympathetic and sympathetic nervous systems influence digestion. This man was in a sympathetic state when he was driving. When he stopped to relax and eat, he found that he could no longer eat the obscenely large quantities of food he had previously eaten; he felt satiated sooner.

It is commonly known that parasympathetic and sympathetic nervous systems antagonize each other. To improve digestion, the parasympathetic nerves cause an increased flow of blood to the intestines, resulting in more nutrient absorption into the blood stream. The sympathetic nerves exert an opposite effect: they constrict the blood vessels around the intestines to shunt them to the muscles in order provide adequate nutrients required for the fight or flight response.

In this man’s case, the sympathetic state he was in while driving inhibited his awareness of satiety. When we are relaxed, the Vagus nerve sends a signal to the parietal cell in the stomach to produce acid. The acid our stomach not only helps break apart food, but it activates enzymes like pepsinogen to pepsin so that it can break apart proteins into amino acids. If our Vagus nerve(parasympathetic) is antagonized by the sympathetic nervous system, protein passes from the stomach into the intestine without being digested into smaller amino acids.

Here is the point: I-cells located in the small intestine sense amino acids and long chain fatty acids. When this happens, these cells secrete a hormone cholecystokinin which—according to endocrinologists–promotes “meal termination and reduces meal size.”[2] If proteins are not sufficiently digested, the I-cells have a more difficult time sensing satiety and don’t secrete cholecystokinin; meal termination does not stop until the mechanical feeling of distention is present.

Dr. Lichtenstein reports that the man could no longer eat his 6 cheeseburgers and whole chocolate cake each meals. Naturally, when he ate fewer quantities of food, the number of bowel movements decreased as well. The man later went on to change his diet and begin an exercise program. This in only one mechanism involved in satiety. There are many others that influence satiety.


[1] Lichtenstein, Brad. “Cheeseburgers and a Chocolate Cake.” Unified Energetics. Volume 3. Summer 2007. 36-40.

[2] David G. Gardner, Dolores Shoback. Greenspan’s Basic & Clinical Endocrinology. 9th Edition. The McGraw-Hill Companies, Inc. 2011. Table 20-1.

Stress and Diabetes

In Uncategorized on September 19, 2013 at 3:42 pm

I was seated across from the patient in what most people consider a typical exam room: uncomfortable chairs, white walls, a small counter with sink & faucet, and an exam table; however, there was something different about this clinic that was apparent to both the patient and the practitioner. It was my second time visiting with this patient.  I had only been on a rotation with Dr. Ryan Bradley at the Diabetes and Cardiovascular Wellness Clinic in for a few weeks, and  already noticed tremendous improvement in his clients.  The patient that was seated in my exam room had type II diabetes for nearly a decade before he had come to visit our clinic. Previous to that day, there was no need for additional care; his blood-sugar levels had been well-controlled on Metformin and a sulfonylurea.

We both knew what was different about this clinic: it was the treatment approach[1]. The management of medications and screenings were similar; however, the foundational therapies of exercise, diet, and stress management were taught and emphasized almost as much as the drug therapies. I asked him why he came to see us that day. He frankly replied that “a close friend had passed away recently and that he wanted to get healthier”.

In our discussion I also learned that for some inexplicable reason, his blood sugars had recently suddenly risen to such an extent that his endocrinologist appropriately prescribed insulin. “What was it that caused this change?”, I wondered. It wasn’t until the second visit that my question was really answered. We had begun reviewing and adding dietary modifications while introducing stress management therapies.

“What does stress have to do with diabetes?”, he asked. It was clear that he saw the correlation between diet and exercise with Type II diabetes, but the effect stress  had on diabetes was not so apparent.

I explained that our bodies have increased levels of cortisol in response to stress, and that stress can decrease our body’s sensitivity to its own insulin[2]. With that brief explanation, I saw a light bulb turn on. He had an epiphany. He explained that at about the same time his blood sugars had skyrocketed, his business(he was a small business owner) had plummeted and gone bankrupt.

I think it unlikely that his course of diabetes was only caused by stress. But, like most chronic disease, the etiology was due to a multitude of factors(stress, diet, exercise, family history, drug tolerance, pre-existing disease, etc) that altogether over extended periods of time put him over the top.

For my physiology students, I would like to explain in more detail how cortisoI influences blood sugar. Cortisol(a hormone produced in the adrenal cortex)  is an endogenous glucocorticosteriod. Exogenous glucocorticosteroids also exist in the form of common medications like prednisone.  Coritsol is secreted in response to stressful events and traumas.  Epinephrine is a hormone that also may be secreted at times of acute stress. When our fight or flight response is turned on, our adrenal medulla secretes more epinephrine into the blood stream. These two hormones are secreted in times of stress.

Cortisol, glucagon, and epinephrine are three hormones that exhibit what is called synergism.  Each of these alone would mildly elevate blood-sugar; however, the combined effects of the three is greater than the sum of each hormone individually.  The physiology text we use gives a great diagram of this specific example.[3]The Best Practice  & Research Clinical Endocrinology & Metabolism recently published an article that included an explaination on how cortisol, glucagon, and epinephrine contribute to hyperglycemia:  “High cortisol levels increase hepatic glucose production, and stimulate protein catabolism and increased circulating amino acids concentration, providing precursors for gluconeogenesis. . . epinephrine stimulates glucagon secretion and inhibits insulin release by pancreatic b-cells”[4].

In other words, the liver produces and secretes sugar into the blood instead of storing it; insulin sensitivity is impaired, resulting in decreased uptake of sugar from the blood; and glucagon secretion is increased causing a synergistic effect with cortisol and epinephrine.

Lifestyle modification is one of many effective tools used in management of type II diabetes. Most clinical studies have analyzed the effectiveness of diet, exercise, and stress management together, while not studying stress alone. Needless to say, the mechanism for cortisol’s effect on increasing blood glucose is established.

 

 

 


[1]Erica B. Oberg,, Ryan Bradley, Clarissa Hsu,Karen J. Sherman, Sheryl Catz, Carlo Calabrese, and Daniel C. Cherkin

Pratibha V. Nerurkar. “Patient-Reported Experiences with First-Time Naturopathic Care for Type 2 Diabetes”.

PLoS One. 2012; 7(11): e48549.

 

[2] Farnoosh Farrokhi, Dawn Smiley, Guillermo E. Umpierrez. “Glycemic Contron in non-diabetec Critically Ill Patients”. The Journal of Clinical Endocrinology and Metabolism. 1993 Nov;77(5):1180-3.

 

[3] Dee Unglaub Silverthorn. Human Physiology An Integrated Approach. 6th Edition. Pearson Education Inc. 2013. 226