Fight The Resistance to Win the War on Fat
If you’ve been reading my blog at all in the past year, you already know I feel very strongly that being fat is a result of eating too many carbs. Contrary to popular 1980′s beliefs, such as staying in the “fat burning zone helps you get lean” using “nautilus machines will build tons of muscle” and “avoid eating fat to lose weight” are all myths that just need to right here and right now. The study below is just proof that it’s taking a while for everyone to catch up with this.
Getting lean and staying lean is all about manipulation of Insulin, the body’s primary instrument in controlling blood sugar. Keep Insulin quiet and you will create an environment that is conducive to fat loss, not just weight loss. Control insulin the rest of your life for a long term strategy in health, fitness and looking good naked. Don’t get me wrong: at certain times Insulin can be very helpful (gaining muscle, for instance) but for the most part you can throw out all your old ideas of starvation when it comes to diet, and instead adopt a sensible carbohydrate restriction in order to lose fat and regain your health.
So why does eating too much sugar make us fat? Think of blood sugar like milk. Milk isn’t necessarily bad, but leave it sitting around long enough on the counter and you have a foul, stinky and stomach churning mess on your hands. Glucose is the same. We need it to function optimally but too much left in the blood stream for too long will cause damage to nerves, arteries and delicate tissue like our eyes (diabetics know all too well the effects of uncontrolled blood sugar on limb loss, nerve damage and loss of vision). So it’s Insulin’s job to sweep up this stuff and keep our blood sugar at a perfectly controlled level. Insulin does this by opening the door to our cells (muscle, liver, fat cells all have keyholes that unlock with the key insulin) and shuttling that excess sugar in. Depending on the type of cell, that sugar can be used to restore glycogen or it can be used for energy, or converted to triglycerides (fancy term for fat).
Everything works well for a while, until cells begin to get so gorged with sugar that they simply don’t want to store anymore. Insulin comes knocking but those cells leave the lights off and pretend not to be home. More Insulin pours into the bloodstream to try and kick down the door, and while this may work for a while, eventually even that fails and so does our ability to continue to produce enough Insulin to keep this fight up – and thus begins the disease of diabetes.
So how do we control this? How do we stop this vicious cycle from destroying our bodies? We stop eating so many carbs. We exercise. Both of these two strategies combined will put an end to most people’s grief when it comes to the debilitating diseases of obesity, metabolic syndrome and diabetes. So why hasn’t the medical community jumped on board with this? Why are there still medical doctors prescribing low fat diets to sick people who need to avoid sugar? In a simple word, grains. Our entire agricultural industry in America depends on us continuing to consume large amounts of starchy cereal grains. There are lobbyists working hard to protect their financial interest and they’ve resisted this topic so much they’ve funded studies to “prove” that whole grains are healthy and that we need to consume large amounts every day or we will shrivel up and die.
It’s taken a long time to get where we’re headed now, but I’m excited, very excited to see the medical community waking up and recognizing that the key to controlling obesity is controlling Insulin, and the best way to do this is to limit carbs.
So why isn’t the Atkin’s diet becoming more popular then? Well for one reason, it’s just so extreme. Look, if you’ve eaten a diet anywhere close to the typical American diet you are probably consuming 200-400 grams of carbohydrate a day. Going from 200 grams to 10 grams a day is going to cause major withdrawal symptoms.
What I suggest to everyone now, is to limit your carb intake to 100 grams a day. That’s still quite a bit of carbohydrate, enough to not feel crappy on, and just enough to ensure you stick with it for long enough to see results. When can you stop “dieting” like this? As soon as you want to get fat again. It’s that simple. Our bodies were never designed to eat more than about 100 grams of carbohydrate a day without paying up on the consequences of that kind of diet. Sure, you can even get away with a splurge on the weekend once you’re at a maintenance weight. But keep the carbs tight and you will be incredibly happy with the results, without losing your mind like you can on an Atkin’s type diet.
Here’s a sample meal that will get you started.
8 ounce Filet Mignon
Steamed Broccoli, Carrots and Cauliflower with just a bit of butter and garlic salt to taste.
Serving of Almonds
Large Orange.
Now, to some of you who are used to eating out of a brown paper bag, this may look like torture. But to those of you who have attempted the Atkin’s diet only to go nuts or completely numb-skulled, then this is a feast for a king. I challenge everyone this new year to reset your pleasure sensors. Re-sensitize your pallette again to the simply sweet foods nature has to offer and you’ll be on the road to looking and feeling great.
Mt Sinai J Med. 2010 Sep;77(5):511-23.
Insulin resistance in obesity as the underlying cause for the metabolic syndrome.
Gallagher EJ, Leroith D, Karnieli E.
Mount Sinai School of Medicine, New York, NY.
Abstract
The metabolic syndrome affects more than a third of the US population, predisposing to the development of type 2 diabetes and cardiovascular disease. The 2009 consensus statement from the International Diabetes Federation, American Heart Association, World Heart Federation, International Atherosclerosis Society, International Association for the Study of Obesity, and the National Heart, Lung, and Blood Institute defines the metabolic syndrome as 3 of the following elements: abdominal obesity, elevated blood pressure, elevated triglycerides, low high-density lipoprotein cholesterol, and hyperglycemia. Many factors contribute to this syndrome, including decreased physical activity, genetic predisposition, chronic inflammation, free fatty acids, and mitochondrial dysfunction. Insulin resistance appears to be the common link between these elements, obesity and the metabolic syndrome. In normal circumstances, insulin stimulates glucose uptake into skeletal muscle, inhibits hepatic gluconeogenesis, and decreases adipose-tissue lipolysis and hepatic production of very-low-density lipoproteins. Insulin signaling in the brain decreases appetite and prevents glucose production by the liver through neuronal signals from the hypothalamus. Insulin resistance, in contrast, leads to the release of free fatty acids from adipose tissue, increased hepatic production of very-low-density lipoproteins and decreased high-density lipoproteins. Increased production of free fatty acids, inflammatory cytokines, and adipokines and mitochondrial dysfunction contribute to impaired insulin signaling, decreased skeletal muscle glucose uptake, increased hepatic gluconeogenesis, and β cell dysfunction, leading to hyperglycemia. In addition, insulin resistance leads to the development of hypertension by impairing vasodilation induced by nitric oxide. In this review, we discuss normal insulin signaling and the mechanisms by which insulin resistance contributes to the development of the metabolic syndrome. Mt Sinai J Med 77:511-523, 2010. © 2010 Mount Sinai School of Medicine.
PMID: 20960553 [PubMed - in process]
