February 8, 2016
The cause of insulin resistance is not well understood. Everyone knows that insulin is a hormone that acts like a key to unlock your cells and let glucose into the cells. Insulin resistance causes the lock and key not to work, even when your body produces more insulin when glucose levels rise in your blood.
Often you will not experience symptoms for varying lengths of time. You will not know that you have insulin resistance. People with severe insulin resistance sometimes develop dark patches of skin on their necks, elbows, hands, and armpits. Your chances of becoming insulin resistant go up if you're overweight, don't get enough exercise, have high blood pressure, or you smoke.
Your blood system may also increase the chances of having insulin resistance, including low HDL (good) cholesterol, high levels of triglycerides in your blood, heart disease, and blood vessel disease in your neck or legs. People with an African American, Hispanic/Latino, Native American, Asian American, or a Pacific Islander heritage are more likely to become resistant to insulin. If your parent, brother, or sister has type 2 diabetes, your risk is higher. If your mother had diabetes while she was pregnant with you (gestational diabetes), your risk also goes up as does the risk for your mother.
The test for insulin resistance is complicated and uncomfortable, so instead, your doctor will probably test you for prediabetes (blood glucose levels that's higher than it should be, 100 to 125 mg/dl). A lab can check the level of glucose in your blood after you haven't eaten for a while, or find an "average" blood sugar level for the past few months. Numbers that are higher than normal suggest you're insulin resistant.
It's hard on your pancreas to keep cranking out extra insulin to try to get glucose into your body's cells. Eventually, the cells that make insulin can burn out, leading to prediabetes and type 2 diabetes. If you catch insulin resistance early and make changes to your lifestyle, you may stop that from happening.
Cut back on sweets, refined grains, and have lots of low carb vegetables and fruits. That kind of eating plan will help you get to and stay at a healthy weight. It also helps your cells use insulin better. The low carb, high fat (LCHF) way of eating, for people with high blood pressure, is a good example. It helps to reduce salt amounts, too. It can lower insulin resistance, especially if you slim down and become more active while you're at it. Studies have also shown a link between low vitamin D and your body not using insulin well.
Physical activity goes a long way toward fighting insulin resistance. Like a healthy way of eating, it helps you lose weight. Exercise also helps your cells use insulin, especially in your muscles. Aim for at least 30 minutes of activity a day, most days of the week. Your heart should beat faster, and you should breathe a little harder.
Lifestyle changes are the best treatment for insulin resistance. But, if you have the condition and are very likely to get type 2 diabetes, your doctor may also want you to try the drug metformin. It can prevent or delay type 2 for younger, heavier people with a very high chance of getting it. Metformin may also help hold off type 2 for women who've had gestational diabetes.
Insulin resistance is part , but not all, of this condition. People with metabolic syndrome have at least three of these traits: a large waist, high triglycerides, low HDL cholesterol, high blood pressure, and blood glucose that is higher than normal. It raises your chances for diabetes, heart disease, and stroke.
I will not go into the technical side of insulin resistance, as a LCHF way of eating can really help in raising HDL, lowering triglycerides, lowering blood pressure, and improving health.
February 7, 2016
There is terminology that is often confused and often not for the right reason. Ketosis, ketones, ketoacidosis, and ketogenic are often misunderstood and confused.
A lot of people are confused by the term "ketosis." You may read that it is a 'dangerous state' for the body, and it does sound abnormal to be "in ketosis." But, ketosis merely means that our bodies are using fat for energy. Ketones (also called ketone bodies) are molecules generated during fat metabolism, whether from the fat in the guacamole, you just ate or fat you were carrying around your middle. When people eat less carbohydrate, their bodies turn to fat for energy, so it makes sense that more ketones are generated.
Many people eat fewer carbohydrates to put their bodies into 'ketosis' to burn fat for energy. Some of those ketones (acetoacetate and ß-hydroxybutyrate) are used for energy; the heart muscle and kidneys, for example, prefer ketones to glucose. Most cells, including the brain cells, are able to use ketones for at least part of their energy. But there is one type of ketone molecule, called acetone, that cannot be used and is excreted as waste, mostly in the urine and breath (sometimes causing a distinct breath odor).
If we have enough acetone is in our urine, it can be detected using a dipstick commonly called by the brand name Ketostix (though there are other brands, they are still often called Ketostix). Even though everyone is generating ketones continuously, this detection in the urine is what is commonly called "ketosis." (Less commonly, but more accurately blood ketones can also be measured.) The higher the concentration of ketones in the urine, the more purple the sticks will turn.
The Atkins Diet in particular advises people to monitor ketosis as an indication of fat burning. Other reduced-carbohydrate diets don't pay as much attention to this, or aren't low enough in carbs to make much of an impression on the sticks. The latter type of diet is sometimes called a "nonketogenic" low-carb diet, and there are many benefits to be had from low-carb diets, even if they are not ketogenic.
Why do some people think ketosis is a bad thing?
There are several reasons people point to as proving that ketosis is a state to be avoided.
#1) Not enough glucose. There is an assumption among some advice-givers, especially registered dietitians, that if a body is burning a lot of fat for energy, it must not be getting "enough" glucose. However, there is no indication, from studying people on reduced-carbohydrate diets, that this is the case. Although it's true that our bodies can't break fat down into glucose (though, interestingly, they easily use extra glucose/carbohydrate to make fat, and not the good kind), our bodies can convert some of the protein we eat into glucose. Indeed, this works well for people who don't tolerate a lot of sugar, because this conversion happens slowly so it doesn't spike blood glucose.
#2) Negative symptoms at first. Another thing that people often point to as a negative thing about ketosis is that people can suffer symptoms such as headaches and dizziness in the first few days of a ketogenic diet. Also, athletic performance can suffer until the body adapts to using fat for energy instead of glucose. This is called keto-adaptation. These symptoms are temporary, but they are often used as "proof" that it's bad to eat a very low-carb diet, as if people are likely to have to tolerate headaches for the rest of their lives if they eat a low-carb diet. In fact, people often find that they have better mental function after keto-adaptation than they did when they were eating a lot of carbohydrates. This is the reason registered dietitians say you need carbohydrates for brain fuel and many CDEs follow the same logic.
#3) Confusion: Ketosis vs. Ketoacidosis. A dangerous condition called ketoacidosis can develop in those with type 1 diabetes, and it is sometimes confused with normal ketosis. The body usually avoids this state by producing insulin, but people with type 1 diabetes are unable to produce insulin. Even most people with type 2 diabetes who inject insulin usually produce enough insulin of their own to prevent ketoacidosis.
February 6, 2016
The following are general guidelines for ketogenic diets:
Carbohydrate - Most of what determines how ketogenic a diet is how much carbohydrate is eaten, as well the individual's own metabolism and activity level. A diet of less than 50 or 60 grams of net (effective) carbohydrate per day is generally ketogenic. However, athletes and people with healthy metabolisms may be able to eat 100 or more grams of net carbohydrate in a day and maintain a good level of ketosis, while an older sedentary person with Type 2 diabetes may have to eat less than 30 net grams to achieve the same level.
I personally do well on 30 to 50 grams of carbohydrates per day. A nutritionist supports me in planning the carbohydrates to not overdo the total and take me out of ketogenic.
Protein - When people first reduce carbohydrates in their way of eating, it doesn't seem as though the amount of protein they eat is as important to ketosis as it often becomes later on. For example, people on the Atkins diet often eat fairly large amounts of protein in the early stages and remain in ketosis. However, over time some (perhaps most) people need to be more careful about the amount of protein they eat as the bodies of many people seem to "get better" at converting protein into glucose (gluconeogenesis). At that point, each individual needs to experiment to see if too much protein is throwing them out of ketosis and adjust as necessary.
Fat - Most of the calories in a ketogenic diet come from fat, which is used for energy. The exact amount of fat a person needs to eat will depend on carbohydrate and protein intake, how many calories they use during the day, and whether they are losing weight (using their body fat for energy). Depending on these factors, somewhere in the range of 60-80% of calories will come from fats on a ketogenic diet (even up to 90% on, for example, the Ketogenic Diet for Epilepsy). People tend not to overeat on diets this high in fat, so calorie counting is rarely necessary.
When eating this large amount of fat, you can imagine that the types of fats consumed are very important. Many authors advise steering clear of oils that are high in polyunsaturated omega-6 fats (soy, corn, cottonseed, safflower, etc). Dr. Stephen Phinney, who has been doing research on ketogenic diets since the 1980's, has observed that people don't do as well when they are consuming a lot of these oils (mayonnaise and salad dressings are a common source). This could be because omega-6 fats can be inflammatory, especially in large amounts, or some other factor, but people didn't feel as well or perform as well athletically in his experiments.
On the other hand, fats high in medium-chain triglycerides, such as coconut oil and MCT oil are often encouraged, as these fats are easily turned into ketones by the body. In general, people on the ketogenic way of eating tend to consume a lot of foods high in monounsaturated and saturated fats such as olive oil, butter (often butter from grass-fed cows is recommended), avocado, and cheeses. The "high oleic" types of safflower and sunflower oils (but not the regular forms of these oils) are also good choices, as they are high in monounsaturated fats and low in polyunsaturates. This way of eating also avoids canola, soybean oils, and other vegetable oils.
I would seriously urge everyone to stop using the term diet to refer to ketogenic way of eating. Call it a food plan or better yet name it “way of eating” because this is something you need to do if you have type 2 diabetes. Diets often fail and are short-term at best and with the problems discussed in 'Part 1' (yesterday's blog), you will need to use this for the long-term.
February 5, 2016
When reading or hearing about low-carb diets, you may have heard the term 'ketogenic diet'. Increasingly, people have questions about this. Are all low-carb diets ketogenic? Is that a good thing or a bad thing? What constitutes a ketogenic diet? What are the advantages and disadvantages of a ketogenic diet? And, there are more questions.
The biggest factor in whether or not a diet is ketogenic is how low in carbohydrates it is. It also depends on how many carbohydrates are consumed on a day-to-day basis. Some people can be ketogenic for several days and then consume a few too many carbohydrates and need to start over to get back into a ketogenic state.
A moderate reduction in carbohydrate can be very helpful to many people, but it won't be ketogenic. Basically, there are three approaches to low-carb eating, only one of which focuses on ketosis as a goal throughout the diet. Diets such as the Atkins Diet start out as a very low-carb ketogenic diet, but as people add carbohydrate, many or most will be eating too many carbohydrates to be in ketosis.
It is probably more accurate to talk about "the degree to which a diet is ketogenic" rather than "whether or not a diet is ketogenic". I will cover ketosis in a future blog so I will not cover it here.
A source of confusion is that there is a transition period while the body is adapting to using fats and ketones instead of glucose as its main fuel. There can be negative symptoms during this period (fatigue, weakness, light-headedness, headaches, mild irritability), but they usually can be eased fairly easily. Most are over by the first week of a ketogenic diet, though some may extend to two weeks. Athletes who closely track their performance may notice more subtle effects up to 6-8 weeks from the start of the diet, and there is some evidence that it may take even longer, up to 12 weeks, for 100% adaptation.
Ketogenic diets are becoming more popular, and for a variety of reasons. In addition to weight loss, they are beginning to be studied as a treatment or prevention for other conditions. They are already well established as a treatment for epilepsy, and researchers are interested in uses for other neurological conditions. A June 2013 paper in the European Journal of Clinical Nutrition listed the following conditions as possibly being helped by ketogenic diets:
- Overweight and Obesity (weight reduction)
- Type 2 Diabetes
- Cardiovascular Risk Factors (particularly improving triglycerides, HDL cholesterol, and patterns of LDL cholesterol most associated with arterial plaque)
Emerging Evidence (some evidence with more research in progress)
- Neurological Diseases other than epilepsy, including Parkinson's Disease, Alzheimer's Disease, narcolepsy, brain trauma, and amyotrophic lateral sclerosis
- Polycystic Ovarian Syndrome
- Some types of cancer (especially, perhaps, some types of brain cancer)
In addition, some athletes are experimenting with using a ketogenic diet to enhance endurance.
February 4, 2016
Bad guidelines don't just give bad advice but they also harm science and impede research. The new U.S. Dietary Guidelines are a perfect example of why we need to have fewer, shorter, and better guidelines. Guidelines should be used only when there is overwhelming evidence and near universal consensus.
Many readers are probably already aware of the most obvious kind of harm inflicted by bad guidelines. Bad advice leads to bad actions. The best example of this is that the earlier guidelines demonizing fat and dietary cholesterol. This has played a significant contributing role to the obesity and diabetes epidemic.
But, there is another sort of unintended consequence that is less obvious and rarely discussed, though it may well be equally harmful. By their very nature, the dietary guidelines present the illusion of successful science, the appearance that clarity and understanding has been achieved by the experts. When this happens, science is the victim.
One of the dangers of the dietary guidelines is that they are viewed as a victory by those that put them together. Then with the HHS and USDA putting an official sign of approval on them, all incentives to perform new research is put aside. For many people, looking at the hundreds of footnotes in a guideline, they would be hard pressed to expend more resources on a topic already supposedly well understood and proven.
A key to making progress is acknowledging how much we don't know and not trumpeting false knowledge. It is important that health organizations need to publicize how much is still unknown. This would instantly give them more genuine credibility, and would also serve to educate the general public about how science works and open the door to the need for more research.
In the end there are only a few public health policies on diet and lifestyle that we can recommend as a society in order to have credibility and so we have to choose them very carefully and focus on the ones for which we have the best evidence and those, which are most feasible. It is important that when new evidence emerges, guidelines should be re-evaluated objectively "rather than people or organizations digging in, and refusing to consider new evidence even when it may challenge one's own thinking. Policy must be based on reliable evidence and not on personal positions.
But another way that guidelines are bad for science is the forced, oversimplification of complex data into simple, often binary treatment recommendations. It is understandable from a practice standpoint to desire simple rules, but scientifically one loses much information by using binary cut points and oftentimes, journal and grant reviewers not only believe that an issue is 'settled' when it is not, but that the thresholds used in guidelines represent a biologically meaningful cut points, when they may have been used for expediency only.
February 3, 2016
The American Diabetes Association (ADA) has officers that are harming people with type 2 diabetes. Dr. Robert Ratner, chief scientific and medical officer for the ADA, is the doctor doing much of the harm to type 2 patients on oral medications. Dr. Ratner does not recommend blood glucose testing, but relying on the A1c test when you have a doctors appointment.
Studies have found glucose fluctuations and daily glucose control are something people with type 2 diabetes are often not aware of and may need to consider. For the many Americans living with type 2 diabetes, A1c is an important metric as it is a key clinical measure of a person's glycemic control over a two to three month period. A controlled A1c level, typically a level at 7 percent or less, has been shown to be associated with a reduction in risks for microvascular complications and cardiovascular events.
While A1c levels are a key component of determining long-term glycemic control, they provide very little information about blood glucose fluctuations that occur throughout the course of a day. A person with type 2 diabetes can experience substantial glycemic excursions following meals. Although there is no prospective clinical trial evidence, there is broad and robust experimental and epidemiologic evidence supporting the concept that excessive glycemic excursions may contribute to long-term risks. In the absence of confirmatory clinical trials, however, direct cause and effect remains controversial.
This points to the urgent need for research and trails exploring the results of daily testing on patients with type 2 diabetes and what these excursions may mean to the health of the patients. Testing programs need to be developed that will demonstrate the importance of blood glucose testing, especially self-monitoring of blood glucose (SMBG). There is much that needs to be accomplished to undo the actions of people like Dr. Ratner.
It is important for people with type 2 diabetes to be aware of glucose fluctuations throughout the day. As patients and physicians become more aware of excessive glucose excursions, both dietary and therapeutic strategies can be implemented to reduce these fluxes. Studies have shown an optimal treatment regimen not only helps bring patients' A1c to goal. It can also help improve daily glucose control throughout the day. Improved glycemic control helps reduce severe fluctuations that have been linked to short-term complications, and which may also lead to long-term microvascular complications and cardiovascular events.
Antidiabetic agents may reduce daily fluctuations and help patients achieve levels of glucose control within the normal range throughout the day. A1c is and will remain a key measure of glycemic control, but as understanding of diabetes grows, the quality of glycemic control may also become an important marker of treatment success.
While I agree that these are important reasons for people to know the importance of blood glucose testing, very few trials consider this in conjunction with low carb, high fat meal plans that can prove very beneficial in lowering the glycemic excursions to hyperglycemia and hypoglycemia. Most doctors ignore the teachings of Dr. Richard Bernstein and his 'law of small numbers' in the treatment of diabetes.
February 2, 2016
While this is research, six experts have a convincing argument for a change in the diabetes classification system. Type 1, type 2, and LADA do not provide clear guidance for diagnosis and treatment of patients with diabetes. The experts in the American Association of Clinical Endocrinologists (AACE) claim that their algorithm is sufficient, but not that accurate.
The new method would make β-cell centric classification of diabetes a single common denominator for all types. At present, the classification identifies only four types of diabetes mellitus. These are type 1, type 2, 'other specific types' (which include genetic defects of beta-cell function, genetic defects in insulin action, diseases of exocrine pancreas and more) and gestational diabetes.
Since the first distinction between presentations of the disease from back in January 1936, the categorization of diabetes has been through numerous changes in order to keep up with new research and findings on the best way to help patients combating the disease. However, the inherent setback with the currently established system lays in the fact that it is inadequate with the present understanding of the phenotypes associated with diabetes. In addition, this and
the limited research and information present at the time of formulating the current system, the designations related with the different types of diabetes are vague and inaccurate. Due to this fact and current evidence-based practice, there is a call to revise the current classification of diabetes mellitus and focus on a β-cell centric classification schema, according to a new article published online in Diabetes Care Jan. 21, 2016.
Based on new research performed by Stanley Schwartz and affiliates, there is a new proposition for using a β-cell centered model for diabetes, which supports the notion that all diabetes originates from an abnormal pancreatic β-cell. Type 1 diabetes has been thought of as an ailment of low insulin production, while type 2 has usually been of insulin resistance. This discrepancy is not clear or helpful. Schwartz and colleagues suppose all diabetes is a product of impairment to beta cells (which produce insulin) and according to this theory, insulin resistance just reveals the rudimentary deficiency in insulin production.
Presently, only about one-third of individuals with insulin resistance will go on to develop diabetes. The basis of the new classification system is treatment of patients as individuals though currently most prescribers will initiate treatment based on a diagnosis instead of the person.
Schwartz believes that diabetes is rooted to β-cell and because of this, classification of diabetes types should be based on causes of that damage so physicians will know how to go about treatment. This “β-cell centric” criterion recognizes that β-cell damage can be caused by inflammation, immune actions, gut biome, high fatty acids, high glucose levels, genetics and other causes; categorization founded on these sources can help cultivate an improved treatment strategy, as opposed to simply knocking down an individual’s glucose level.
Defining key markers and the processes of care in using them will allot appropriate patient-centric approaches with either currently established medications or an up-and-coming drug.
This proposed model acknowledges a total of 11 interconnecting pathways that contribute to hyperglycemia, which are prompted by the transformation of genetic predispositions to insulin resistance. These pathways of hyperglycemia contribute to β-cell dysfunction within the liver, adipose, brain, colon, immune dysregulation and muscle. The “damage caused results in downstream hyperglycemia arising from increased glucagon secretion, as well as a reduction in insulin production, incretin effect and amylin levels.” For any one patient, the routes for hyperglycemia vary and more than likely involve numerous pathways. It is significant to note that these arbitrating pathways of hyperglycemia are common across prediabetes, type 1 diabetes, type 2 diabetes and other outlined forms of the disease state.
The most ideal management model presented was the impression that treatment should comprise the use of the least amount of agents to help in targeting the greatest number of these particular mediating pathways of hyperglycemia in any given patient. The research also noted that any treatment option that would potentially be detrimental to the long-term integrity of the β-cells–specifically including sulfonylureas and glinides–should be avoided because any potential benefits of the medications are severely outweighed by the risks associated with their use. It will be very interesting if the ADA will even consider this as important, but it should be very important.
February 1, 2016
At first, I had passed on this topic, but after a discussion with Scott Johnson about this and his promotion on his blog, I feel that I need to write about the public service advertising (PSA) about prediabetes.
Another type 2 blogger has also blogged about this, but was very negative in her thoughts. She may be correct in her thinking, but I feel that the campaign is on target and I have seen two of the ads. Yes, they are over the top in a way, but with all the noise of political ads, I feel that the promotion will do more good than harm. It needs to be shocking and use language that will capture people's attention.
In discussing this with Scott, he made some excellent observations and I have his permission to use them. Scott says: (and I agree)
“- Something with this much attitude is certain to upset some. Totally expected.
- I'm trying to keep in mind the intended audience for these messages. It's not us. These are TV commercials designed to grab people's attention in the midst of all the other media noise. A tough job.
- With that in mind, do we really think a piece about diabetes in the tone we're used to seeing would do anything? I don't.
- If these can catch even a few people among the many who will ignore them, it's helping more than hurting.”
In this year of political ads and their constant noise, I do hate to have the TV and even the radio on during the ads. This is why I don't feel that the PSA's are that offensive.
Losing weight and being healthier are at the top of most everyone’s New Year’s resolutions. But, despite the best intentions, work, kids, and social events often push lifestyle changes to the bottom of the list. While many are familiar with type 2 diabetes, fewer are aware of prediabetes, a serious health condition that affects 86 million Americans (more than 1 in 3) and often leads to type 2 diabetes. People with prediabetes have higher than normal blood glucose (sugar) levels, but not high enough yet to be diagnosed with type 2 diabetes.
To raise awareness and help people with prediabetes know where they stand and how to prevent type 2 diabetes, the American Diabetes Association (ADA), the American Medical Association (AMA), and the Centers for Disease Control and Prevention (CDC) have partnered with the Ad Council to launch the first national public service advertising (PSA) campaign about prediabetes. The PSA campaign, featuring first-of-its-kind communications techniques, was developed pro bono by Ogilvy & Mather New York for the Ad Council.
Nearly 90 percent of people with prediabetes don’t know they have it and aren’t aware of the long-term risks to their health, including type 2 diabetes, heart attack, and stroke. Current trends suggest that, if not treated, 15 to 30 percent of people with prediabetes will develop type 2 diabetes within five years. The good news is that prediabetes often can be reversed through weight loss, diet changes and increased physical activity. Diagnosis is the key.