Wednesday, April 9, 2014

HOW A PLANT BASE DIET CAN LEAD TO PERMANENT DAMAGES TO OUR HUNGER/SATIETY CONTROL SYSTEM


I am still under shock after reading the recent article that was all over Internet last week stating: “Vegetarians are less healthy (in terms of cancer, allergies, and mental health disorders), have a lower quality of life, and also require more medical treatment.”
But what did upset me the most is the conclusion of the researchers: they still advocate a vegetarian diet or, at least, a “meat free day for all” during the week and, of course, staying away from dreadful “animal fat”… even if this well done observational study brings in numbers that says clearly the contrary…
We already know anyone eating 50 g fructose per day (equivalent of 2-1/2 apples per day…) for one month will develop a Metabolic Syndrome with all the consequences related to this disease….
But let’s look now at another interesting subject: how a “plant based” diet can screw up permanently our “hunger/satiety” system. Yes, and I will repeat it: PERMANENTLY!!!
We all well know Leptin is the lookout hormone - the gatekeeper of fat metabolism - monitoring how much energy an organism takes in. It surveys and maintains the energy balance in the body, and it regulates hunger.
Leptin is secreted by fat cells and is received by receptors in the hypothamus. If leptin is absent, feeding is uncontrolled and relentless. In normally healthy people, if leptin is present and receptors are sensitive, feeding is inhibited.
More body fat means less food is required, and so leptin is secreted to inhibit feeding and the accumulation of excess adipose tissue. Overweight people generally have higher circulating leptin, while leaner people have lower leptin levels. Leptin also responds to short-term energy balance. A severe caloric deficit will result reducing secretion of this hormone – this is your body’s way of getting you to eat when you need energy. It’s the hunger hormone. Overfeeding temporarily boosts leptin, reducing hunger.
Put simply: long-term, leptin signals that the body has adequate adipose tissue (energy) stores; short-term, this hormone signals that the body has had enough to eat. Both are supposed to result in the reduction in appetite.
But why are so many people so overweight? Why don’t overweight people respond to all that circulating Leptin and curb their food intake? And if they’re overfeeding, why isn’t the resultant Leptin increase having an effect? They shouldn’t be hungry, but they are. There’s a disruption of the Leptin pathway and this is what we will look at.
Something is causing the Leptin receptors in the hypothalamus to down regulate (Leptin resistance), or something is blocking the Leptin from reaching the receptors. Either way, this mechanism isn’t working as it should.
So what’s causing the breakdown of the Leptin pathway? Take a look at wild animals. They eat varying amounts of food, sometimes gorging, sometimes fasting, but never counting calories. And yet these animals seem good at maintaining an excellent body composition.
All signs, it seems, point to Leptin, especially its sensitivity, as being dependent on the dietary environment we provide. As long as they do not stay far from their evolutionary diets, wild animals do not have damaged metabolisms. On the other side, most modern humans having stayed FAR AWAY from their evolutionary diets, are metabolically deranged, with misguided or disrupted Leptin pathways.
When Leptin was discovered, it was hailed as the key to the obesity epidemic. Researchers figured if they could just administer it to the obese folks, appetite would be curbed and food intake would reduce. It actually worked for some people, but it was expensive (about $500 per day) and unsustainable, and for others, it had no effect. Now we know this is because these folks were Leptin resistant…
How do we maintain adequate levels of Leptin – enough to keep from going mad with hunger – without growing resistant to its effects? There are many causes but the two main ones are FRUCTOSE and LECTIN, substances related to plant food.
Let’s look first at fructose.
In rats, fructose feeding inhibits Leptin receptors, meaning Leptin has no effect. Interestingly, rats on a fructose diet gained more weight EVEN WHEN switched to a high-FAT diet.
Fructose appears to affect the Leptin pathway in two ways. First, fructose directly renders the hypothalamus resistant to Leptin. Normally responsive receptors in the brain have a muted, or even silent, response to leptin when fructose intake is high. Second, high blood triglycerides – brought on by a high fructose intake – block the passage of Leptin to the brain. High triglycerides actually physically prevent leptin from passing through the blood-brain barrier, and the leptin that does get through elicits a poor response from the receptors.
As we all know, a high-fat, low-carb, low-fructose diet generally decreases serum triglycerides and increases satiety; perhaps the lower triglycerides are allowing more Leptin to pass through and inhibit hunger.
As for LECTINS, especially those from cereal grains are direct causes of Leptin resistance. Wheat germ agglutinin (a lectin present in wheat, barley, and rye) actually binds directly with the Leptin receptor and prevents from working properly. The inability of the receptors to bind describes Leptin resistance.
Lectins are abundant in raw legumes and grains, and most commonly found in the part of the seed that becomes the leaves when the plant sprouts, aka the cotyledon, but also on the seed coat. They’re also found in dairy products and certain vegetables.

Lectins in plants are a defense against microorganisms, pests, and insects. They may also have evolved as a way for seeds to remain intact as they passed through animals’ digestive systems, for later dispersal.

Lectins are resistant to human digestion and they enter the blood unchanged. And because we don’t digest lectins, we often produce antibodies to them. Almost everyone has antibodies to some dietary lectins in their body. This means our responses vary. Certain foods can even become intolerable to someone after an immune system change or the gut is injured from another source.

Some experts hypothesize that it’s no coincidence the top allergens also contain some of the highest amounts of lectins (including: dairy, wheat, soy, peanuts, tree nuts, fish and shellfish).

Not all lectins react with human cells, but vegetables with lectins that do react include tomatoes, potatoes, string beans, zucchini, green peas, asparagus, radish, sweet peppers, cucumber seeds and mushrooms. Other human-reactive lectins are in the sprouts of soybeans, mung bean and lentils. One zucchini, for example, may contain more lectin than a zucchini from another location or one harvested at another time. These vegetables can be eaten raw, as their lectins are not orally toxic. However, if you are lectin-sensitive you will find these vegetables easier to digest when they are cooked.
Some fruits contain lectins that cause human blood cells to clump together, or agglutinate. This includes cherries, pomegranate, grape seeds, raspberry seeds, apples, watermelon, grapefruit, banana, lemon, orange, strawberries, currants and plums.

Grains that contain lectin include wheat germ, rice germ and barley germ. Some spices contain lectins including garlic, marjoram, allspice, nutmeg and peppermint. Cocoa beans, Arabica coffee beans, walnuts, hazelnuts, sesame seeds and sunflower seeds also contain human reactive lectins.

So it is not surprising why so many folks that got obese on “high-plant diet rich in fructose and lectin” have now to live the entire existence with a “broken metabolism”…

Denis

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