Читать книгу The Italian Reset Diet - Dario Polisano - Страница 17

Premise

As mentioned in the chapter on the Mediterranean Diet, nutrition has changed a lot over the years. When we reflect on our ancestors’ diet, and how it was based around meat, fish, vegetables, eggs, dry fruits/nuts, and only sporadically fresh seasonal fruit, we can picture the sheer disruption that our bodies have had to endure over the years. New food products are present now on the market, which we consume in excess because we are convinced that our wonder-sack—the stomach—is always ready to work for us on absolutely anything. No one ever told us that all foods contain proteins and lectins which communicate with our DNA and immune system, and which can cause the entire body to go haywire, causing serious pathologies. In this chapter, we will analyze the molecules and foods to fear the most, since, according to my experiences and studies, they are the most devastating of all.

Gluten

Gluten is a macromolecule consisting essentially of proteins from some varieties of cereals, and responsible for cellular toxicity phenomena. Their mechanisms, to date, remain largely unknown. These consequences occur in a significant portion of the population with a complex symptomatology described using the term celiac syndrome or celiac disease. For a long time, the symptoms of the gastrointestinal tract have been used almost exclusively as a tool to formulate diagnoses, prognoses and therapeutic courses with regard to the disease. The acquisition of further knowledge regarding pathogenetic mechanisms and diagnostic markers and monitoring has made it clear that many other zones and functions, in addition to those of the gastrointestinal system, may be affected by this complex pathology. Taking this into consideration, a much larger number of people are diagnosed with celiac disease; for example, the functioning of the immune system, the musculoskeletal development of the individual, and some neurological aspects are part of modern clinical investigation protocols. The prestigious medical journal “The Lancet” reiterates the following in an article: “to improve diagnoses, the medical belief that sensitivity to gluten is an exclusively intestinal disease must change.” Furthermore, this new knowledge has allowed us to highlight, in some cases, phenomena that cannot be identified as a real food intolerance, but rather as a so-called “sensitivity” to gluten. By being a real problem for a large number of people, this “sensitivity” is attracting increasing attention in the clinical and nutritional fields.

Wheat, barley, rye, spelt, kamut and oats all belong to the cereal family. These food products have always been, and still are, the basis of the Western diet. Their main protein is gluten, which, as mentioned before, is a macromolecule, consisting of two proteins (known as gliadin and glutenin) which tend to form chemical bonds in water, giving dough elasticity and resistance. Because of these characteristics, in recent years the industry has increased the quantities of gluten in our wheat through genetic selections. The first was made in the 1950s on Cappelli wheat, which was first irradiated with y-rays and then crossed with Mexican CIMMYT wheat. From this selection, Creso wheat was born, followed by many others. To date, there are many species of wheat, and these selections have spurred the increase in celiac disease.

Celiac disease is an autoimmune disease of the small intestines that occurs with the introduction of gluten in genetically predisposed individuals. Celiac disease is a genetically transmitted disease that can affect members of the same family. The manifestation of this pathology occurs following a weakening of the body, such as an instance of influenza, surgery, etc. The percentage of people affected by celiac disease is about 1 percent, meaning one out of every hundred suffers, but the data collected in recent years on the expansion of the phenomenon and its variability shows that among these hundred people there would be many who have the disease but will never be diagnosed and just go on living with it.

However, as the chemist Lorenzo Acerra tells us in his book Mal di Glutine (“Gluten Ache”), celiac disease is not a recent pathology, as it began around 10,000 years ago at the end of the last ice age, when man could no longer find enough game, and started cultivating wheat plants. This was a fundamental moment in the development of the first civilizations—in fact, by being able to stay in the same place, man led a more sedentary and less difficult life, guaranteeing a demographic explosion. The generations to follow, however, had a different body structure from their ancestors; they were shorter, less muscular, and were also more affected by bronchitis, pneumonia, osteoporosis and periodontitis. Then there was the advent of new infectious diseases, such as tuberculosis in Egypt. Today we realize that these were the consequences of the introduction of cereals into human nutrition, meaning their diets were very different from those of their ancestors. Cereals are foods rich in starches that give acidity, fermentation, and glycemic and insulin peaks. They are composed of lectins, the glycoproteins used by plants to defend themselves from attacks by insects. Therefore, lectins are capable of damaging the intestinal mucosa once they come in contact with it Cereals are also composed of gluten, a very different protein from the animal proteins to which the human intestines used to be more accustomed.

Gluten was, and still is, a protein that cannot be completely digested, because man does not have the proper enzymes for it. Enzymes are the “workers” of our intestines, involved in the reduction of macromolecules into simple molecules. In gluten, amino acid bonds cannot be split individually and, therefore, small protein chains with high inflammatory power are formed. The symptoms of celiac disease vary from person to person. Organs distant from the digestive system may also be affected. In children, there is a prevalence of gastrointestinal symptoms, such as swelling and diarrhea, but at times also constipation, nausea, vomiting, foul-smelling stools and weight loss. An obvious sign of this disease in children is short stature with a delay in growth, due in particular to poor absorption, which can lead to serious deficiencies, especially with respect to vitamins and minerals. Because of this, we witness iron deficiency anemia, osteoporosis, depression and anxiety. In adults, the symptoms are not only gastrointestinal in nature. They are very varied and can affect various organs. We can come across epilepsy, depression, headaches, stomatitis, miscarriages, infertility, herpetiform dermatitis and many more. Many people live with the disease without realizing it, but unfortunately, the longer the diagnosis is delayed the more these patients risk suffering long-term consequences.

Celiac disease is a multifactorial pathology in which various causes, from environmental to genetic, contribute to the development of this autoimmune disease. The environmental factor is represented by exposure to gluten. Genetic factors affect several genes, but those genes have only been spotted in a small percentage. You got it right—the classic genetic analysis of celiac disease is not entirely accurate in diagnosing this pathology. The most relevant genes in the development of the disease are currently identified as HLA II DQ2 and DQ8, and they are located on chromosome 6. It must be emphasized that these genes are present in 40% of the healthy population. We must ask ourselves then: is this population really healthy, or is it silently developing gluten problems that can suddenly explode into some pathology? In any case, other genes have been identified, and among these there is the Celiac2 locus on chromosome 5q31-33, Celiac3 on the 2q 33 region, and the recently identified Celiac4 locus.

In the diagnosis of celiac disease, various types of analysis are addressed, ranging from the search for IgA and IgG anti-gliadin antibodies (gliadin is a part of gluten), anti-transglutaminase and anti-endomysium, to intestinal biopsies for the evaluation of the intestinal villi’s health state.

If the analyses metioned above turn out negative, but typical symptoms of the pathology still exist, and if one or more family members are celiacs, the next step in the procedure is a genetic analysis of the HLA DQ2 / DQ8 profile. Positive test results indicate an increased probability of manifesting the disease, but do not give a sure result, given that 40% of the population still has these genes. Therefore, according to conventional medicine, one should make do with the symptoms of the pathology and continue to consume gluten, until the pathology explodes in the intestines with the flattening of the villi. This is odd, considering that they usually give statins to diabetics, even with low cholesterol, for the prevention of atherosclerotic plaques. Prevention, apparently, is good only if we need to take drugs, but if it is a question of changing one’s dietary regimen, then it is not allowed anymore! I consider even more absurd the fact that the Mayo Clinic, one of the most prestigious American medical institutes, informs us how some patients with negative HLA DQ2 / DQ8 results, without the presence of antibodies, may present symptoms typical of celiac disease—a situation due to genetic predisposition with the association of the HLA DQ-α1 HLA DQ-β1 system in the class II region, which activates only the immune response of T lymphocytes, with a consequent lack of the formation of the specific autoantibodies of celiac disease. In summary, gluten is silently destroying a person's body, but as there is no clear laboratory data, then that person can calmly continue to poison himself. This very situation, which is presently studied and well-known in the scientific field but not widely recognized (for reasons I cannot understand), is known as gluten sensitivity. It is a syndrome characterized by multiple intestinal and/or extraintestinal symptoms, which occur shortly after consuming gluten. These symptoms improve or disappear after the elimination of gluten in subjects for whom the celiac disease diagnosis has been excluded. The first detections of this pathology took place in the 1980s, when female patients were described as having symptoms, credited to celiac disease or irritable bowel syndrome, that would at first disappear with the elimination of gluten and then reappear with its renewed intake. These women were thought to have psychological issues, and were treated with antidepressants!