What if increasing your salt intake actually improved your diabetic blood sugar?
What if increasing salt intake actually lowered your blood pressure? Could it be that easy?
Just about every patient that I see has significant worry about salt intake. Some greater than others. In fact, some people are so salt phobic that when I encouraged its use, they called me a “quack” and left my practice. But does salt restriction really work, 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 18 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine. Granted, it is a small sample of people, only 21 in the study. However, the results are profound.
21 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
What was noteworthy was that those with insulin resistance and diabetes had improvement in their glucose levels while on sodium supplementation. Those with hypertension had improvement in their blood pressure while on the sodium supplementation. Lastly, 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, 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 what I, also, have seen clinically in my practice for over 13 years.
We know that the average human needs 3 grams of sodium per day and 3 grams of potassium per day. If you’re eating the standard American diet (SAD diet) including processed foods, you’re getting 2-3 grams per day of sodium. In fact, the CDC claims the worst meals for you are:
Bread
Processed chicken dinners
Pizza
Pasta
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. This is the cause of the keto-flu I wrote about a few weeks ago. 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 1/2 – 2 teaspoons of salt per day. I like Redmond’s RealSalt or if you can’t find it, Himalayan Pink Salt, because the pink sea salts contain sodium, potassium, magnesium and zinc.
Could it be that salt restrictions are making our insulin resistance and blood pressure worse? That’s what the clinical evidences are pointing toward. However, more research is still needed.
Want to know more about a ketogenic life-style? Click the link on KetoLife above 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 Supplement section above 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!
Watch as we discuss how a ketogenic diet lowers your blood pressure . . . yes, fat drops blood pressure to normal ranges. We talk about the four mechanisms causing blood pressure to rise and how ketosis improves those mechanisms. . . pull up some pork rinds (Pork Clouds are my favorite) and guacamole and enjoy . . .
Hypertension (elevated blood pressure) is one of the triad symptoms of metabolic syndrome. Most of the hypertension that I see clinically is driven by insulin resistance as the underlying cause. I see this problem in a very large majority of the people in my office and I am seeing people younger and younger show up with continually increasing blood pressure.
In medical school, we were taught to treat “borderline” or “slightly elevated blood pressure,” through “lifestyle changes” which was another way of saying exercise, caloric restriction & hold the salt. But most physicians today will tell you that exercise, salt & caloric restriction doesn’t work. When asked why the 34 year old male in my office suddenly has elevated blood pressure, the only explanation we had was it is a “genetic problem,” or “blood pressure naturally goes up as we get older,” or “you’ve been eating too much salt,” and they are started on blood pressure medication and sent on their way. But, as time went on, I found that I had to keep adding more and more blood pressure medication to control the continually rising blood pressure of the patients in my practice.
Most of these people will have a progressive elevation in blood pressure over time, and these blood pressure (anti-hypertensive) medications are/were continually raised until the person is on four or five different blood pressure pills at maximal doses. Again, when questioned why, their genetics are blamed and that is the end of it. Or is it?!
What shocked me was that when I took patients off of salt & caloric restriction, and placed them on low carbohydrate high fat diets (and yes, I gave them back their salt), their blood pressure normalized. I noticed that as their fasting insulin levels began to fall, their blood pressure began to return to normal.
What?! Blood pressure rise is caused by insulin?!
Ummm . . . Yes!
I am a prime example. During the first few years of my medical practice and reserve military service, we had routine vitals checkups. I was working out 3-5 days a week with weights and running 3-5 miles 2-3 times a week and restricting my calories to 1500 per day. So, I thought I was in pretty good shape. However, it was not uncommon for for the nurse to raise her eyebrows at my blood pressure readings in the 140-160 systolic and 85-98 range diastolic. “Oh, it’s the lack of sleep last night,” or “it’s the caffeine I had this morning,” would be my excuse. But I was making a lot of excuses, and in light of those excuses, my caloric restriction, exercise and salt restriction, I was also still gaining weight.
By the 5th year of my medical practice, I weighed 60 lbs heavier than I do today and I struggled to keep my blood pressure under 150/95. I was violating my own counsel . . . don’t trust a fat doctor for nutritional advise. (Or, was that advise from Dr.House?)
After cutting out the carbohydrates (I’ve kept my carbohydrate intake < 20 grams per day), moderating my protein intake and eating all the fat I am hungry for each day, my recent physical examination at the beginning of June 2016 revealed my blood pressure at 112/64. I don’t remember ever having blood pressure that low. And to be honest, I didn’t sleep well the night before my exam due to a number of middle of the night patient calls.
When I first started treating the insulin resistance problem in the human, rather than the blood pressure problem, I began to see immediate reductions in blood pressure within one to two weeks. So much of a reduction that if I didn’t warn the patient that they should begin to back down their blood pressure medications, they would experience symptoms of dizziness, light-headedness, headache and a few patient’s nearly passing out. On a low-carbohydrate, high-fat (ketogenic) diet you need salt (sodium, potassium, & magnesium). The process of burning fat as fuel causes you to lose increased amounts of sodium & potassium, and you have to replace these electrolytes. A number of my patients begin a low-carbohydrate, high-fat diet and are afraid of increasing their salt intake. Not replacing these electrolytes while on a ketogenic diet can also lead to low blood pressure, dehydrate and dizziness.
I often wondered why applying a ketogenic diet had such a profound effect on blood pressure so quickly. Dr. Robert Lustig helped answer that question for me.
In order to understand how the Standard American Diet (we call it the SAD diet in my office) raises your blood pressure, it is important to understand how the body processes the basic sugar molecule. Sugar is one glucose molecule bound to a fructose molecule. This is broken down in the body and 20% of the glucose is metabolized in the liver, the other 80% is sent on to be used as fuel throughout the body. Fructose, however, is where the problems arise. 100% of the fructose is metabolized in the liver, and the by product of fructose metabolism is increasing the liver’s production of MORE glucose and the byproduct of uric acid. Uric acid is produced and this inhibits the production of nitric oxide. The diminished nitric oxide in the presence of an increased level of glucose (stimulating increased insulin production due to eating starches) constricts the blood vessels and raises blood pressure. Yes, that donut you just ate raised your blood pressure for the next 12 hours.
The mechanism that fructose containing carbohydrates, sugars and starches raise blood pressure, cholesterol and cause weight gain can be seen in the really complex diagram found in Dr. Lustig’s 2010 article:
So, how do you lower your blood pressure through diet?
First, cut out all the simple sugars. These include anything with table sugar, high fructose corn syrup and corn syrup. (This is why people with any change in diet see some improvement in weight and blood pressure as they remove the simple sugars like candy, sugared drinks and pastries from their diet.)
Second, limit your overall intake of other sources of carbohydrates including any type of bread, rice, pasta, tortilla, potato, corn and carrots. Realize that carbohydrate in fruit is fructose, and when taken with other forms of glucose can have the same effect as table sugar – it can and will raise your blood pressure, as well as halt or cause weight gain.
Third, if you are taking blood pressure medications for hypertension, see your doctor about close monitoring of your blood pressure as it can and will drop within 2-4 weeks of making these dietary changes.
Maintaining ketosis is really important for weight loss and blood pressure or hypertension control. I am very much an advocate of using real food for this process, but I have also found that the use of exogenous ketone salts aid significantly in maintaining ketosis. I have found that exogenous ketones are the next step in bridging the difficulty of day to day maintenance of ketosis.
It isn’t making the mistakes that’s critical; it’s correcting them and getting on with the task that’s important. If you’ve been calorie restricting and exercising to lower you blood pressure, don’t fret. A simple change in your diet focused on restricting starches and carbohydrates has been demonstrated in my office to be more powerful than many of the blood pressure medications we’ve used for years.
85% of the people that walk through my office doors have some degree of insulin resistance.
What is “insulin resistance?” It is an over production of insulin in response to ANY form of carbohydrate intake (yes, even the “good carbs” cause an insulin over-response in a person with insulin resistance.)
How do I know this? Because I routinely check insulin levels (I check them every three months) and the down stream markers of insulin on a large number of the patients that I see. I have been fascinated by the fact that a diet high in both sugar and fat [like the Standard American Diet, (SAD) diet] turn on the genetics leading to insulin resistance. Starch and sugar load the genetic gun.
Insulin acts like a key at the glucose doorway of every cell in your body. In many people, the insulin signal is blocked by hormones produced in the fat cell and the the insulin, acting like a “dull or worn out key” – can’t open the glucose doorway as efficiently.
So, the body panics, and releases extra insulin in response to the same load of carbohydrate or glucose. People with insulin resistance will produce between 2-20 times the normal amount of insulin in response to a simple carbohydrate load. Recent studies(1, 2) reveal high cholesterol and diets high in both fat and carbohydrate cause insulin resistance to progress or worsen.
So, instead of producing enough insulin to accommodate the one slice of bread or the one apple that you might eat, the insulin resistant person produces enough insulin for an entire loaf of bread or an entire bushel of apples. This excess insulin then stimulates one or all of the following:
Weight Gain – Insulin directly stimulates weight gain by activating lipoprotein lipase to take up triglycerides into the fat cells. This causes direct storage of fat and increases your waistline. (3)
Elevated Triglycerides – Insulin directly stimulates production of free fatty acids and triglycerides through hepatic gluconeogenesis and is even more notably amplified by the broken signaling mechanism of the FOX-01 phosphorylation mechanism in patients with insulin resistance. (4)
Increased number of Small Dense LDL (sdLDL) particles – Low density lipoprotein (LDL, or “bad cholesterol”) is actually comprised of various sized lipoproteins including small, medium and large. As triglycerides increase, the small dense LDL particle numbers increase. Research points to the fact that it is the small dense particle that is highly atherogenic (leading to the formation of vascular plaques within the arteries). (5, 8)
Elevated Uric Acid – Leptin resistance and insulin resistance syndromes are often found together and are suspected to have significant influence on each other. High insulin loads lead to “sick adipose cells” causing leptin resistance. This has a dramatic effect on hepatic fructose metabolism increasing the production of uric acid. Excess insulin suppresses urinary excretion of uric acid and dramatically increases serum content of uric acid and the risk of kidney stones and gout. (6, 7)
Increased Inflammation – Increased levels of circulating insulin have a direct correlation on raising many of the inflammatory markers and hormones including TNF-alpha and IL-6 in the body (9). Any disease process that is caused by chronic inflammation can be amplified by increased circulating levels of insulin including asthma, acne, eczema, psoriasis, arthritis, inflammatory bowel and celiac disease, etc.
Elevated Blood Pressure – Increased uric acid production from insulin resistance as noted above directly suppresses production of nitric oxide within the vasculature and increases blood pressure (7). This completes the triad of metabolic syndrome (elevated triglycerides & cholesterol, weight gain, and elevated blood pressure) found in patients with insulin resistance.
Water Retention – We have known for many years that insulin affects the way the kidney uses sodium in the distal nephron. Insulin has a direct effect on sodium retention in the kidney. As insulin levels rise, the kidney retains increased levels of sodium (10). Water follows sodium and thereby causes fluid retention. This is the reason that many of my insulin resistant patients who have struggled with leg swelling and edema suddenly improve when they correct their diet and their high circulating insulin levels fall. It is also the reason that many of my patients show up in my office after the holidays with swollen legs and amplified swelling in their varicose veins after cheating on their ketogenic diets.
If you are plagued by any or all of these, my first suggestion is to see your doctor and get screened for insulin resistance. I treat patients with these every day and have reversed these effects in thousands of patients with the correct diet and/or medications. Having seen these signs and patterns over the last 20 years of medical practice, I am still astonished every day by the dramatic effect our diet plays on the hormonal changes within the body. Remember that the food you eat is actually the most powerful form of medicine . . . and the slowest form of pernicious poison.
Cholesterol Elevation Impairs Glucose-Stimulated Ca2+Signaling in Mouse Pancreatic β-Cells, Endocrinology, June 2011, Andy K. Lee, Valerie Yeung-Yam-Wah, Frederick W. Tse, and Amy Tse; DOI: http://dx.doi.org/10.1210/en.2011-0124
Glucose-Stimulated Upregulation of GLUT2 Gene Is Mediated by Sterol Response Element–Binding Protein-1c in the Hepatocytes, DIABETES, VOL. 54, JUNE 2005; Seung-Soon Im, Seung-Youn Kang, So-Youn Kim, Ha-il Kim, Jae-Woo Kim, Kyung-Sup Kim and Yong-Ho Ahn
Selective versus Total Insulin Resistance: A Pathogenic Paradox, Cell Metabolism, Volume 7, Issue 2, 6 February 2008, Pages 95–96, Michael S. Brown, Joseph L. Goldstein
Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy, Gentile M, Panico S, et al., Clinica Chimica Acta, 2013
Sugar, Uric Acid and the Etiology of Diabetes and Obesity. Diabetes. 2013;62(10):3307-3315, Richard J. Johnson; Takahiko Nakagawa; L. Gabriela Sanchez-Lozada; Mohamed Shafiu; Shikha Sundaram; Myphuong Le; Takuji Ishimoto; Yuri Y. Sautin; Miguel A. Lanaspa
Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep;110(9):1307-21. doi: 10.1016/j.jada.2010.06.008. Lustig RH
Cardiovascular Risk in Patients Achieving Low-Density Lipoprotein Cholesterol and Particle Targets. Atherosclerosis. Vol 235; 585-591, May 2014, Peter P. Toth, Michael Grabner, Rajeshwari S. Punekar, Ralph A. QuimboMark J. Cziraky c, Terry A. Jacobson
Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome The Insulin Resistance Atherosclerosis Study (IRAS), Circulation, July 2000, 102:42-47; Andreas Festa, MD; Ralph D’Agostino, Jr, PhD; George Howard, DrPH; Leena Mykka¨nen, MD, PhD; Russell P. Tracy, PhD; Steven M. Haffner, MD
The Effect of Insulin on Renal Sodium Metabolism. Diabetologia. September 1981, Volume 21, Issue 3, pp 165-171. R. A. DeFronzo