High ‘bad’ cholesterol helps the virus in all sorts of ways, but eating the right foods can enhance your immunity – fast!
Covid-19 results in severe pneumonia, which progresses to acute respiratory distress syndrome (ARDS) in 5% of cases. Severe Covid disease is associated with high mortality among the elderly (over 70) and in patients with pre-existing chronic conditions.
The chronic conditions are confined to metabolic syndrome and include obesity, diabetes, high blood pressure, heart disease, stroke and dementia. A high cholesterol level is the common factor in all of these conditions. And cholesterol accumulates in lung tissue over time.
Therefore, high cholesterol is the single most important factor in predicting the severity of Covid-19 infection in the high-risk groups.
Conditions presenting with high cholesterol include metabolic syndrome (as discussed above), an underactive thyroid, environmental toxicity, infection, gut dysbiosis and leaky gut.
If you are diagnosed with high cholesterol, more tests need to be carried out, tests such as SIBO, GI-MAP, thyroid and toxic elements panels and genetics. The hepatic biliary disease may be part of hyperlipidaemia. look for fat deposition around the eyes (xanthelasma), on the eye (arcus Senlis), or on tendons (xanthoma). The prevalence of aortic calcification and aortic stenosis (AS) varies from 30 to 40% in this group compared with 0.2% in the general population.
This article discusses the combination of Covid and cholesterol as a recipe for severe Covid disease since most patients presenting with this clinical scenario require intensive therapy care. We will also review the growing evidence in the medical literature that Covid-19 thrives only in an environment (host body) rich in cholesterol. This is because high cholesterol not only enhances the viral infectivity but also lowers the host’s immunity, resulting in severe disease and poor clinical outcome.
The cholesterol family
The lipid panel requested by your doctor informs you about the various fat components in your blood. These include total cholesterol, triglyceride, very low-density lipoprotein (VLDL), low-density lipoprotein (LDL) – also known as the bad guy – and high-density lipoprotein (HDL) – the good guy.
The lipoproteins act as vehicles to transport cholesterol around your body. For example, LDL distributes cholesterol to various body tissues, whereas HDL works in the opposite direction, collecting damaged (oxidised) LDL to be cleaned up in the liver.
High total cholesterol and high LDL exacerbate Covid infection and can result in poor clinical outcome. This is due to the lowering of the protective immunity and the over-reactivity of the immune system, resulting in severe pulmonary and systemic inflammation.
Cholesterol is a major component of the immune cell membrane. Excess cholesterol lowers the protective immune response and ignites the immune system’s over-reactivity, resulting in the well-known cytokine storm, the pathological feature of severe Covid disease, which is associated with very high mortality.
The Covid-19 virus is a collection of RNA nucleic acids enclosed in an envelope made up of cholesterol. This makes cholesterol an essential element for viral assembly, replication and infectivity.
A case report showed the lowering of high cholesterol and LDL at the onset of Covid infection. The patient required mechanical ventilation, and his cholesterol was back to a high level in 60 days. Clinical patterns suggest that a significant fall in cholesterol and LDL could be an early sign of severe Covid disease.
Another study observed 28 severe cases to show the downward regulation of apolipoproteins during the transition of Covid-19 from mild to severe illness, and the decrease of APO A -1 during persistent inflammation.
On the other hand, studies reported low HDL as an independent risk factor for severe Covid disease. HDL is an anti-inflammatory lipoprotein that protects against oxidised LDL. It is also involved in immune regulation during Covid-19 infection.
Low apolipoprotein (APO A-1 and APO E) may lead to disease progression and complications due to interference with HDL function.
Cholesterol: facilitating the virus’s entry AND lowering your immunity
Serum cholesterol was significantly lower in Covid patients in China, implying that low cholesterol may predispose us to infectious diseases, since LDL takes part in the immune process to de-activate almost all types of microorganisms.
The anti-infectious property of LDL has been documented in human studies as well. In a meta-analysis of 19 cohort studies including almost 70,000 deaths, Jacobs et al. found an inverse association between serum cholesterol and mortality from respiratory and gastrointestinal diseases.
Another multi-ethnic study, performing a 15-year follow-up of more than 120,000 adults, found an inverse association between initial cholesterol levels and the risk of being admitted to hospital later in life due to an infectious disease.
It makes sense for patients on cholesterol-lowering treatment, who present with a life-threatening Covid-19-infection, to cease their treatment – at least until they have recovered from the infection.
“The mouse trap”: cholesterol and age
Observations at the outset of the pandemic in China noticed that the elderly were vulnerable while children were resistant to Covid-19 infection. The elderly experienced severe life-threatening symptoms with high mortality, while there were no reported deaths among children under the age of 12.
This difference in mortality between the young and old patients was attributed to the age-dependent translocation of cholesterol into the lung cells. Cholesterol entry into the lung cells is known to increase with age.
Animal studies demonstrated an increase in cellular cholesterol store by 45% in 28-week-old mice compared with 8-week-old mice.
Cholesterol increases the sensitivity of the ACE2 receptors and enhances the entry of the virus into the host cells through a process called endocytosis. The presence of cholesterol also encourages virus replication, resulting in severe disease.
Cholesterol enhances infectivity by increasing the virus’s efficiency in entering the host cells in three ways: it increases the number of entry sites; it positions the ACE2 receptors to facilitate viral entrance, and it produces a protein (Furin) that activates the virus membrane for attachment to the entry site.
A high-fat diet increases cholesterol loading by 40% to facilitate virus entry. Low cholesterol disrupts the localisation of ACE2 receptors and reduce the severity of Covid-19. Mortality increases in elderly people and those with chronic metabolic conditions, such as hypertension, diabetes, heart disease and dementia.
Patients on statins, ACE inhibitors or ARBs should keep taking them.
High membrane cholesterol facilitates virus entry. Covid-19 interacts with cholesterol and HDL. Covid-19 patients may present with dyslipidaemia. Statins may interact with Covid-19.
Cholesterol: a Covid severity predictor
Since cholesterol plays a role in regulating the Covid-19 virus’s entry into the host cell, this makes cholesterol and lipoproteins potential markers for monitoring the viral infection status. The lipid profile and the composition of the cell membranes could be targeted to inhibit the virus life cycle, as a new antiviral therapy.
Higher membrane cholesterol coincides with the higher efficiency of Covid-19 entry into host cells. However, patients with Covid-19 were found to have lower levels of blood cholesterol and a lower level of high-density lipoproteins (HDL.)
Scientists observed how the virus merges with a cell to infect it. In a ground-breaking study, researchers watched lab-grown cells with spike proteins interacting with the host cell’s ACE2 receptor. The spike proteins merged with the host ACE2, the two cellular membranes fused, and an opening formed, letting the virus pour its genetic material into the host cell to form a mega cell.
This fusion happens only in a cholesterol-rich environment. Again, high cholesterol was needed to facilitate the virus replications inside the host cell. This is because cholesterol is a very important component of the virus envelope.
Cholesterol is known to be an important factor in a large number of viral infections. The interesting thing is that cholesterol’s role in viral entry varies a lot between viruses. It’s not clear exactly how cholesterol aids Covid-19, but understanding that process could offer clues about the biology of infection.
The cholesterol-dependent mechanism of ACE2 localisation, as well as the virus’s entry, could explain why Covid-19 is so much more lethal in the elderly. Tissue cholesterol levels increase with age, and as a result of chronic disease conditions like atherosclerosis and other acute or chronic inflammations. These are the same conditions that are found to increase the severity and likelihood of symptomatic Covid-19 disease.
Based on these findings, the researchers propose that cholesterol is essential for SARS-CoV-2 infection. Low cholesterol levels provide few entry points, and reduce their size, as in children. However, with ageing, higher cholesterol levels cause more and larger entry points, accounting for the much higher likelihood of infection.
The researchers next attempted to find out whether the reduced viral entry was due to less receptor binding. They tested the binding of the virus to the receptor-binding domain (RBD) of the ACE2 receptor on the culture cells.
Cholesterol increases Furin availability: the virus requires protease-mediated priming to enter the host cell. In SARS-CoV-2, this is performed by Furin, which has a cleavage site between the S1 and S2 subunits of the spike protein.
On the other hand, another site cleaves a fusion peptide and allows the virus to enter.
Study: The role of high cholesterol in age-related COVID19 lethality. Image Credit: Naeblys / Shutterstock
Statins: the double-edged sword
Statin has an antiviral effect as it reduces the synthesis of cholesterol. Again, statins improve endothelial cell function and stabilise atherosclerotic plaques. Muscle symptoms and an increase in liver enzymes limit the use of statin. But statins also increase your risk of type 2 diabetes and dementia.
Statins lower LDL, increasing the severity of Covid-19. Fibrate may be a better option as it increases Sulphatide to reduce the severity of the disease, also reducing triglycerides and increasing HDL.
Statin may promote the inflammatory pathways by increasing IL-18, resulting in severe pneumonia, ARDS and death. Discontinuation of statins, particularly in the elderly people, might be helpful.
By blocking cholesterol synthesis, statins may be able to reverse some of the immunosuppressive effects driven by excess cholesterol.
Increased antibody titre increases after pneumococcal vaccination in patients on atorvastatin, but the adjuvant capacity of statin was lost by chronic use.
Hypercoagulation in Covid-19 may be controlled by the combined therapy of omega-3 and aspirin. Both EPA and DHA have beneficial effects in managing the cytokine storm.
Amid all of the evidence – some of it inconclusive – what we can conclude is that cholesterol – high overall cholesterol, high LDL and low HDL – is bad for us. So, what can we do about it? We are what we eat – and here is a quick checklist of foods that lower our cholesterol and boost Covid-19 immunity.
Food that lowers cholesterol
- Almonds help by raising HDL and reducing unhealthy LDL. This should be consumed in moderation in view of the high-calorie fattening content.
- Avocado is great in lowering LDL and TG and raising HDL.
- Nuts contain polyunsaturated fatty acids that keep your cholesterol in check.
- Whole grains contain fibre that is effective in lowering LDL cholesterol.
- Beans and legumes take longer to digest and leave people feeling full for longer – a great option for weight loss.
- Fruit and vegetables are rich in fibre that lower cholesterol absorption.
- Blueberries are rich in antioxidants, reduce levels of LDL, and are of equal benefit whether taken fresh or frozen.
- Dark chocolate prevents LDL from being oxidised or damaged.
- Dark leafy greens, such as kale and spinach, which include carotenoids, are antioxidants and Lutein lowers oxidised LDL to prevent its deposition in arteries.
- Tomatoes contain lycopene antioxidants. You need 30 mg per day.
- Fatty fish or omega 3 lowers LDL and increases HDL.
- Garlic contains powerful allicin, used in fresh garlic and garlic supplements.
- Red wine includes phenolic compounds to reduce LDL.
- Green tea, black tea and white tea contain EGCG, important for lowering blood pressure.
- Quercetin lowers inflammation and allergies.
- Extra-virgin olive oil contains monounsaturated fat, raising good and lowering bad cholesterol.
Foods that boost immunity to Covid-19
- Quercetin in red grapes and red onions, black tea. Cruciferous vegetables.
- EGCG in green tea, onions and garlic, ginger, turmeric.
- Zinc in meat, beans, and nuts and seeds.
- Vitamin C in kiwi fruit, bell pepper, citrus fruit, mango, hibiscus.
- Vitamin D in oily fish, butter, mushrooms and sunshine.
And there we have it, my friends. Cholesterol has always been bad for us in so many ways – and the last year has merely added Covid-19 to the list. I hope you find the above advice useful. Please do let me know any of your thoughts related to cholesterol and Covid-19…………
- Have you been able to lower your cholesterol?
- How quickly?
- Or are you struggling to make inroads?
- Do you feel it has been a factor in your experience of Covid?
Please do not hesitate to come forward with any observations or questions – and, as always, I will be delighted to hear and answer them. Stay safe, eat well, have faith!
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