We are what we eat. And we eat, at least in the Western world, far too much. With the result that we pay more and more for all the consequences. The growing availability of food, together with a change in eating habits and lifestyles – we always move too little – has led to a surge in obesity cases in the last fifty years. This has also been accompanied by an increase in cases of autoimmune diseases. The association between obesity and autoimmune diseases is not accidental: excess metabolic load contributes to altering the metabolism and the functioning of the immune system. To the point that there are those who think they can fight autoimmune diseases by also acting on their diet.
Autoimmune diseases, obesity and overweight as “accelerators”
One of them is Giuseppe Matarese, full professor of immunology and general pathology at the Federico II University of Naples, president of the scientific committee of the Italian Multiple Sclerosis Foundation, who in the journal Science explains how eating habits put your health at risk. And not only with regard to the effects of obesity. “Compared to the seventies, today we ingest up to a thousand more calories a day – she warns – and we are now overexposed to a metabolic load that can translate into hyperfunctioning of the immune system”. Just as happens in autoimmune pathologies, in which the immune system not only defends us from viruses and bacteria, but also directs its action towards the body, hitting any type of organ, Matarese recalls: “Like the pancreas, in the case of diabetes , the brain, in multiple sclerosis, and the joints, in arthritis”. However, blaming the excess of calories only tells part of the story: genetic predisposition and exposure to an environment that is too clean – which does not allow you to train the immune system – are the other pieces of the puzzle, according to Matarese: “ The excess metabolic load was just the accelerator that was missing”.
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Leptin: the hormone that acts as a “bridge” with the immune system
The link between obesity and immune system malfunction is complex and involves the production of molecules and the activation of molecular pathways that we only partially understand. However, one of these has been known for some time: leptin, better known as the satiety hormone, produced by adipose tissue and which regulates food intake. This substance also acts as a bridge between fat and the immune system, explains the researcher: “It controls the ability to defend us against infections.” Thus, in the event that fat decreases, the availability of leptin decreases and the body receives a “saving” signal, which causes it to reduce energy expenditure.
Otherwise, an excess of leptin is associated with an excess of energy availability which favors pictures of hyperactivation of the immune system, just as is observed in the case of autoimmune diseases. Here then is that nutritional condition and defenses are closely related: “We know that in conditions of scarcity of food, of undernutrition, the immune system is not very efficient in fighting infections – continues Matarese – while in the presence of a nutritional surplus we observe the presence of an overactivation of the immune system and inflammation”. With mechanisms in this case involving T lymphocytes: some are driven to produce proinflammatory substances, others, such as regulatory T lymphocytes, responsible for keeping immune reactions at bay by promoting immunological tolerance, decrease. And these cells are actually deficient in obese people for example, the article reads.
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Diet and medications to keep the immune system at bay
Shedding light on these mechanisms is needed to understand how to intervene to try to contain what Matarese almost recognizes as an epidemic of autoimmune diseases. And there are essentially two strategies: on the one hand the dietary ones, which aim to reduce caloric intake, even in a mild way, so as to directly influence the molecular pathways sensitive to energy intake, on the other that of modulating these same pathways through drugs.
Calorie restriction on the one hand and pseudo-starvation therapies, as they are called, on the other. “We are still largely in an experimental field – underlines Matarese – but there is now a lot of evidence to support the benefits of caloric restriction or the use of some drugs, such as metformin, to reduce inflammatory phenomena”. They are those that come from studies conducted in animal models of multiple sclerosis or rheumatoid arthritis, but also in people with multiple sclerosis and metabolic syndrome. These interventions would be capable of reducing inflammatory molecules and promoting the recovery of T reg lymphocytes, but some effects, concludes the researcher, could also be due to the ability of caloric restriction to induce a microbiota with anti-inflammatory capabilities.
To understand whether mild caloric restriction interventions, in addition to a first-line drug (dimethyl fumarate), can improve the efficacy of the therapy, AISM and FISM have funded a study that Matarese is carrying out. “We involved 120 patients with relapsing-remitting multiple sclerosis and the study will continue until next June, when we will then start the follow-up. The data we have collected so far is encouraging,” confides Matarese. Proof that the insights and evidence gathered in animal models are right.