The new generation of injectable weight loss drugs has captured national attention. Of course, it is always helpful to read the fine print. These drugs do cause weight loss, but nearly 40 percent of that loss is lean body muscle. Your metabolic efficiency decreases when you lose lean body mass (like that found in your organs). Consequently, once you stop taking these injectable drugs, the weight loss rapidly returns, but primarily as increased body fat. Essentially, these injectable weight loss drugs are “forever” drugs. Great news for the drug companies, but not so good for the patient because the same drugs cause numerous side effects.
Finding a Dietary Alternative
The first thing is to understand that these injectable weight loss drugs use the metabolic pathways that have existed for millions of years. The second thing to realize is that dietary protein is the natural stimulus for releasing the hormones that suppress appetite. Finally, to achieve fat loss, you must reduce insulin resistance (1). So, could a dietary system providing adequate dietary protein and decreasing insulin resistance provide a pathway for fat loss without losing lean body mass?
Fortunately, such a dietary system has been shown to do that. That dietary system is the Zone diet. The foundation for the Zone diet was first described in my book, The Zone, published in 1995 (2). The basic patent for using the Zone diet to reduce insulin resistance was applied in 1992 and issued in 2000 (3).
Since that time, I have continued to add several dietary enhancements to the basic concept to make the Zone diet an appropriate alternative to Ozempic, Wegovy, Mounjaro, and other potential hormonal-based drugs not only for weight loss but also as a treatment for diseases that are strongly associated with insulin resistance such as type 2 diabetes and heart disease. The term that describes this evolving overall technology is Metabolic Engineering™.
How can the Zone diet increase the hormones that cause satiety?
The essential hormones that cause satiety are released from the gut in response to the protein levels at each meal. If you have adequate protein levels at a meal, these hormones will travel directly to the brain to stop hunger. If you don’t have enough protein at a meal, these satiety hormones will not be released, and appetite quickly returns.
So, what is the right amount of protein you need to consume at every meal?
The answer is about 30 grams of protein. Another benefit of consuming this level of dietary protein at a meal is that it stimulates three additional hormones to suppress hunger as opposed to the current injectable drug approved for weight loss.
Why not consume more protein at a meal for even greater satiety?
There are two reasons. The first reason is that higher protein levels stimulate insulin release from the pancreas. Excess insulin secretion slows down fat loss (1). The second reason is that extra protein overstimulates the gene transcription factor mTOR, inhibiting AMPK activity (4). Furthermore, any reduction of AMPK activity slows down the burning of stored body fat.
The Nutritional Power of Balance
Additionally, you must balance that appropriate amount of protein with the correct amount of low-glycemic carbohydrates to maintain stable blood sugar levels. If the 30 grams of protein at a meal is balanced with carbohydrates rich in fermentable fiber, this allows the production of short-chain fatty acids (SCFA) by gut microbes that further enhance satiety hormones from the gut (5). The best carbs are low glycemic carbohydrates, primarily non-starchy vegetables, just like your grandmother told you to eat.
To maximize the satiety benefits, you will need about 30 grams of protein at every meal, but you will also need about 40 grams of fiber-rich carbohydrates at each meal to generate the maximum satiety effect. This allows short-chain fatty acids (SCFA) by gut microbes that further enhance the release of satiety hormones from the gut (5). . This is the foundation of the Zone diet’s patented ability to reduce insulin resistance, which is the key to losing excess body fat.
References
- Ruderman NB et al. AMPK, insulin resistance, and the metabolic syndrome. J Clin Invest 123:2764-2772 (2013). doi: 10.1172/JCI67227
- Sears B. The Zone. Regan Books. New York, NY. (1995)
- Sears Method of and nutritional and pharmaceutical compositions for reduction of hyperinsulinemia. U.S. Patent No. 6,140,304 (2000)
- Gonzalez A et al. AMPK and TOR: The Yin and Yang of cellular nutrient sensing and growth control. Cell Metab 31:472-492 (2020). doi: 10.1016/j.cmet.2020.01.015
- Christiansen CB et al. The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. Am J Physiol Gastrointest Liver Physiol 315:G53-G65 (2018). doi: 10.1152/ajpgi.00346.2017
Let Us Know What You Thought about this Post.
Put your Comment Below.