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Osteoarthrosis and dietary fats: proofs are “on the plate”, listening to “gut feelings”

Osteoarthritis is the most common version of arthritis and affects millions of people around the world, including about 35 million people in the United States alone. The condition is characterized by the slow breaking of the cartilage, which acts as a buffer between the joints. As cartilage degenerates, the joints can become swollen, stiff and painful and the condition tends to worsen over time. Osteoarthritis can affect any joint in the body, but it is found more often in the knees, hips, hands and spine. Traditionally, osteoarthritis is referred to as a condition of wear – in other words, the joints that are used more often or more heavily are more likely to suffer a constant disruption of the cartilage, eventually leading to osteoarthritis. There are some known risk factors for osteoarthritis – for example, more commonly it affects older people and women are more likely to develop it than men. Likewise, previous injuries to the joints and bone deformities also increase the chances of developing the condition.

Another known risk factor for osteoarthritis is obesity. This is partly due to the excessive stress exerted on the joints when carrying more weight around, but the connection between excess weight and osteoarthritis can go a little deeper. Almost 5 years ago, a team of researchers from Queensland University of Technology and the University of Southern Queensland, both in Australia, studied a connection between dietary fat and the onset of osteoarthritis. This research follows the previous work from the same team who discovered that antioxidants and anti-cholesterol drugs (statins) can slow down the progression of joint damage, attributed to fatty acids found in foods such as palm oil and butter. Saturated fatty acids, infact, trigger oxidative stress in cells that maybe counteracted by some natural antioxidants. In this research project, scientists studied specifically the effects of a diet rich in saturated fatty acids and simple sugars on osteoarthritis. These dietary components reflect the nutritional elements commonly found in junk food: high fats and carbohydrates.

The study shows that osteoarthritis may have less to do with the general use of our joints and more to do with what we eat regularly. According to their results, a diet containing 20% ​​saturated fat and simple carbohydrates produced osteoarthritic changes in the knee. In 2016, the same team discovered a link between leptin, a hormone involved in obesity and some cellular degeneration in cartilage cells (chondrocytes). Leptin was found to be highly expressed in human osteoarthritis. The researchers sought to explore the possible effects and mechanisms of leptin on apoptosis (cell death) and the autophagy of chondrocytes during the onset of osteoarthritis. The expression of the enzyme Lysyl oxidase-like 3 (LOXL3) in the cartilaginous tissues and the concentration of leptin in the synovial joint fluid, was measured in samples of 45 patients with osteoarthritis and 25 healthy donors. The LOXL3 protein was positively regulated in patients with osteoarthritis, which was positively correlated with the concentration of leptin in the synovial fluid.

Therefore if leptin increases LOXL3 in cartilage cells, promoting inflammation, this means that there must be some connection between fat metabolism and cartilage health. The deposits of saturated fatty acids in the cartilage change its metabolism and weaken the cartilage, making it more prone to damage. This, in turn, would lead to osteoarthritis pain from the loss of the shock-absorbing effect of cartilage. Long-term use of animal fats, butter and palm oil seemed to weaken the cartilage of the mice that fed on them. However, when they replaced meat fat with lauric acid – a saturated fat commonly found in coconut oil – the opposite effect was observed: Lauric acid seemed to be beneficial. When the researchers replaced the fat of meat in the diet with lauric acid, they found signs of decreased deterioration of cartilage and metabolic syndrome.

The conclusion was that the replacement of traditional diets containing lauric acid derived from coconut with palmitic acid derived from palm oil or stearic acid derived from animal fat, has the potential to worsen the development of both the metabolic syndrome and osteoarthritis. Most likely shorter chain fatty acids undergo a slightly metabolism compared to regular chain or long-chained fatty acids. It is known that short chain fatty acids may affect ion channels and some cellular enzymes that are not usually affected by long-chain fatty acids This also confirms other team results about the beneficial effect of coconut oil on metabolic profiles. For more about thisn the topic, we suggest more readings on our website www.medicomunicare.com totally dedicated to science topics in english. However, since obesity has shown a clear connection with the state of the intestinal microbiota, some teams of researchers have already explored this hypothesis in animal laboratory models. with good preliminary data.

The association between osteoarthrosis and low-grade systemic and local inflammation is well known. Inflammatory reactions gets worse with regular aging, a phenomenon nicknamed “inflammaging”. According the rationale beneath, osteoarthrosis etiopathogenic mechanisms might include epigenetic alterations, mitochondrial dysfunction, cellular senescence and an age-related increased production of inflammatory mediators. A direct correlation between aging and gut dysbiosis has been previously demonstrated as well, and is mainly characterized by an increase of pro-inflammatory anaerobes species and a consistent decrease in anti-inflammatory species. A possible link between gut dysbiosis and osteoarthrosis might be suggested by the correlation between the serum levels of bacterial metabolites and joint degeneration. This correlation has been described in rodent models and humans and is characterized by increased levels of circulatory inflammatory markers including bacterially produced lipopolysaccharides (LPS).

Slowly, these fat-soluble molecules may cross the gut barrier into the bloodstream anc may trigger a “silent”, invisible yet real inflammatory response which proceeds without fever. LPS, hovewer, stimulate immune cells to produce cytokines like interleukin 1 (IL-1), interleukin 6 (IL-6) and tumor necrosis factor (TNF-alpha), which trigger inflammation in several tissues. Beside this possible hidden cause for cartilage degeneration, this mechanism has been invoked the onset of insulin-resistance and pancreatic beta-cell killing, which may lead to type 2 diabetes. This is why a balanced gut community is central for a general good health. Consumption of fermented foods like yogurt and kefir, a diet with a good ampunts of vegetal fibers and, where chosen, probiotic supplementation will allow this to happen. LPS are produced by aerobia species, which may be slowed down by lactobacilli or lactic bacteria (Lactobacillus, Bifidobacterium, Actinoplanes, ecc.), regular component of fermented or other functional foods.

A 2017 randoized clinical trial proved that probiotic L. casei Shirota supplementation ameliorated knee osteoarthrosis parameters in sick patients, compared to healthy individuals. As further confirmation, a couple of months ago has been officially published a clinical trial demonstrating that the oral administration of another living probiotic (L. rhamnosus) may improve pain and inflammation in the context of hand osteoarthrosis.

  • edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Scientific references

Jhun J, Cho KH, Lee DH et al. Cells. 2021 Apr; 10(5):1057.

Silvestre MP et al. Nutrients. 2020 Nov 12; 12(11):3469. 

de Sire A, de Sire R et al. Nutrients. 2020 Feb 22; 12(2):574.

Henrotin Y et a. Cartilage. 2019 Apr 13:1947603519841674. 

Lei M et al. Benef Microbes. 2017 Oct 13; 8(5):697-703.

Larrañaga-Vera A et al. Arthritis Res Ther. 2017; 19(1):264.

Meo Burt P et al. Endocrinology. 2016; 157(12):4602-4614.

Huang ZM et al. Osteoarthr Cartilage. 2016; 24(7):1246-53.

de Munter W et al. Osteoarthr Cartilage 2016; 24(5):844-55.

Collins KH et al. Osteoarthr Cartilage 2015; 23(11):1989-98.

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Dott. Gianfrancesco Cormaci

Medico Chirurgo, Specialista; PhD. a CoFood s.r.l.
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry residency in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Guardia medica presso strutture private dal 2010 - Detentore di due brevetti sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento enzimaticamente neutralizzata (owner of patents concerning the production of bakery gluten-free products, starting from regular wheat flour). - Responsabile del reparto Ricerca e Sviluppo per la società CoFood s.r.l. (Leader of the R&D for the partnership CoFood s.r.l.) - Autore di articoli su informazione medica e salute sul sito www.medicomunicare.it (Medical/health information on website) - Autore di corsi ECM FAD pubblicizzati sul sito www.salutesicilia.it
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