Are You Doing Everything “Right” and STILL Can’t Lose Weight?
Have you heard about the low carbohydrate (low carb), keto-adapted diet and wonder what it is, how it works, if it is relevant for you, and whether it is a healthful long-term option? Did you know there is no nutritional “requirement” for carbohydrates like there is for protein, fat, or vitamins?
5 Disconnects With the “Low-Fat Message” 
1. The “low-fat message” has been pushed in the popular media and academia for three decades while obesity rates in the United States have grown dramatically.
2. A low-fat diet – even one restricted in calories – is high in carbohydrate, which drives up blood insulin levels. Insulin is a hormone that drives fat into storage (into fat cells) and stimulates hunger. A low carb diet, on the other hand, allows insulin levels to remain low and fat stores to be burned with reduced hunger and cravings.
3. Dietary saturated fat has been demonized in the media, textbooks, and in national policy; published scientific data shows no connection between dietary saturated fat intake and either saturated fat levels in the body or the long term risk of heart disease.
4. The strongest correlation between major dietary and blood levels of saturated fat is with dietary carbohydrate – not with saturated fat intake. On average, the more carbohydrate you eat, the higher the content of saturated fats in your blood.
5. While science continues to uncover the variability of how people respond to diet and exercise, nutrition policy makers persist in preaching a one-size-fits-all high carbohydrate message.
More and more information is coming to light regarding the risks of high carbohydrate consumption and yet the USDA cannot seem to divest itself of this one-size-fits-all sinking ship: the USDA currently recommends a whopping 45-60% of our diets should come from carbohydrate consumption. This is an astounding number, given high carbohydrate intake (refined or not) is clearly shown to cause hyperglycemia and insulin resistance, which can lead to:
• Nerve damage
• Organ damage in diabetics
• Increased mortality
• Increased risk of stroke and heart disease
• High blood lipid profiles
• Weight gain, obesity
• Promotion of bacterial infections and other diseases
• Promotion of cancer progression
• Hastening of aging
• Hardening of the arteries
Every individual is unique due to genetics, ethnicity, age, gender, and environmental factors, which influence how we respond to food. Those with metabolic syndrome and related conditions are carbohydrate intolerant, which manifests as insulin resistance and is associated with high blood triglycerides, high blood pressure, and in its most severe form, type 2 diabetes. These individuals show dramatic improvement when dietary carbohydrates are reduced, which implies the “high carb, low fat” mantra promoted by national policymakers is irresponsible and unrealistic as a one-size-fits-all dietary approach.
“The Art and Science of Low Carbohydrate Living” is an invaluable resource for dissecting fact from fiction and correcting the errors of casually administered low carb diets and the research that studies them.
The purpose of this book is three-fold: providing the reader with historical and evolutionary perspective about low carb diets; explaining how the body responds to low carb diets; and demonstrating how low carb diets are used effectively to treat patients in clinical applications. Like flying to Hawaii, you are not going to fly only half way otherwise you end up in deep water. The same principle applies to the low carb diet: without achieving a keto-adapted state and maintaining it as a lifestyle, you never reach your “island of safety” and the benefits of the low carb approach are lost. Long-term success with the low carbohydrate lifestyle involves much more than simply reducing or cutting off carbs.
The authors, Drs Volek and Phinney, are uniquely qualified authorities on the topic: collectively, they have more than 50 years of research and clinical practice experience with low carb diets and a few hundred published peer-reviewed articles on the topic. They have personally adopted the low carbohydrate lifestyle for many years with great success. In short, this book has the potential to revolutionize nutritional therapy for treating people who struggle with weight gain, obesity, type 2 diabetes, metabolic syndrome, and impaired fasting glucose (or around 100 million Americans), while reducing or eliminating the use of pharmaceuticals to treat these conditions.
What is a Low Carbohydrate Diet?
Low carb diets are define in one of two ways: the first is how you as an individual perceive yourself responding physically to carbohydrate restriction and using your personal experience to determine the level of desired benefit. The second is a physiologic condition where there is a fundamental shift in your body’s fuel homeostatis (i.e., energy regulation) away from glucose as a primary fuel, known as “nutritional ketosis”. When you eat carbohydrates, your body preferentially uses carbohydrates for fuel and stores them as fat. The opposite occurs when you take those carbohydrates away from your diet. That is why when you consume a low carb diet you can increase your level of saturated fat or monounsaturated fat intake two or three times. You are not storing fat, you are burning it.
In the first, whether losing weight and keeping it off or putting a case of type-2 diabetes into remission, how much you limit your dietary carbohydrate intake is driven by your personal experience. This means the amount of carbohydrate that you eat varies considerably (i.e., 25g to 125g per day) depending on your individual metabolic condition and your desired level of benefit.
What is “Nutritional Ketosis”?
Nutritional ketosis is the adaptation of the body’s hormonal set and inter-organ fuel exchange to allow most of your daily energy needs to be met by fat, either directly as fatty acids or indirectly by ketone bodies made from fat. This process begins for most adults when total carbohydrate is restricted to less than 60g per day along with a moderate intake of protein. After a few weeks at this level, the primary serum “ketone” (beta-hydroxybutyrate, or B-OHB) rises above 0.5 millimolar (mM). At this ketone level, which is 10-fold higher than that in someone with a daily intake of 300g of carbohydrate, the brain begins to derive a substantial portion of its energy needs from B-OHB resulting in a commensurate reduced need for glucose.
With further restriction of carbohydrate below 50g per day, the serum B-OHB rises in response to reduced insulin secretion. However, because dietary protein prompts some insulin release, and serum B-OHB itself stimulates insulin release by the pancreas (albeit subtly), adults eating 20 g of carbohydrate and 75-150g per day of protein rarely run serum B-OHB levels above 3mM. This is in contrast to the response to total starvation (i.e., no dietary carbs or protein) where the serum B-OHB levels run as high as 5 mM.
This 10-fold range of serum ketones, from 0.5 to 5 mM, is your body’s normal physiological response to varying degrees of dietary carbohydrate and protein restriction. This response range is called “nutritional ketosis”, and is associated with metabolic adaptations allowing your body to maintain a stable state of inter-organ fuel homeostatis. This process is dependent on an adequate, albeit minimal, ability of the pancreas to produce insulin in response to dietary protein and serum ketones, thus maintaining serum B-OHB in the range where it replaces much of your body’s (and your brain’s) need for glucose without distorting whole-body acid-base balance.
Nutritional ketosis is by definition a benign metabolic state that gives human metabolism the flexibility to deal with famine or major shifts in available dietary fuels. By contract, “diabetic ketoacidosis” is an unstable and dangerous condition that occurs when there is inadequate pancreatic insulin response to regulate serum B-OHB. This occurs only in type-1 diabetics or in late stage type-2 diabetes with advanced pancreatic burnout. In this setting of deficient insulin, when exogenous insulin is withheld, serum B-OHB levels reach the 15-25 mM range, 5 to 10 fold higher than the levels characteristic of nutritional ketosis.
Unfortunately, the general public and even many health care professionals tend to confuse these two distinct metabolic states. Understanding how different they are is critical to being able to capture the many benefits of nutritional ketosis while avoiding the risks in that very small minority of the population subject to developing diabetic ketoacidosis.
