Fatty Lipomas - Support For The Cytokine Theory imageFatty Lipomas - Support For The Cytokine Theory image
Fatty lipomas are discrete sections of fat which form hard or soft lumps, most often subcutaneously, but can be found almost anywhere in the body on rare occasions.

They rarely become cancerous, and to date there's only speculation as to their causes. Cytokines at the site of blunt trauma injuries is one theory. (There is no reason that there couldn't be multiple causes, which could lead to "proving" each of them wrong, by citing that the theory doesn't hold for someone with a different cause, as has happened with Alzheimer's research.)

People with Wilson's disease have a higher rate of fatty lipomas than the general population.

Single fatty lipomas 1:1000 (0.1%) vs 26% Wilson's disease: 260 times more common.

Several = 0.02% vs 16 of 80: 20% Wilson's disease. 1in 5,000 vs 1 in 5, a 1000 to 1 ratio.

Wilson's disease is described as a copper storage disease. It might be easier to understand for the layperson as an inability to get rid of copper via the normal route, ceruplasmin taking copper out through yhe liver as bile, instead causing the body to deplete zinc to "carry" copper out through the kidneys.

This leads to low zinc. Coronavirus has highlighted the fact that low zinc can result in a cytokine storm, an immune system issue which here is suggested as causing problems leading to fatty lipomas, encapsulated fat tissue which looks and feels like hard or soft lumps, as a result of improper healing after a blunt injury to the fat cells.

While most conditions have more than one cause, many causes will have something in common. For the layperson, think of a broken leg. Generally, the cause for broken leg will be some sort of impact, or some sort of grabbing on both ends and twisting or bending, or severe osteoporosis so that using it normally actually breaks it. But in all cases, it has to do with the bone being over stressed for its current strength. On top of that, an impact could be from a baseball, a car, or the edge of a curb if someone falls. A number of causes, but something in common.

(Due to the conditions mentioned in this particular document, and others, I use a cell phone and have problems sometimes editing. I have noticed that there are mistakes of a minor sort in this document. This is still being edited, but I need this information out for my doctors. Please do your best to translate or ignore the minor mistakes. I had an editor before Coronavirus.)

Then there is the two-factor viewpoint. If one doesn't have osteoporosis, it's a lot harder to break a leg. Strong bones require more force to damage them. Two factors, weakened bones plus a significant but not severe impact, might be necessary to cause the symptom of a broken leg.

Some conditions might require more than one factor to be in place before they will occur. Again, one must always be aware that there's liable to be exceptions and other causes.

I propose that the reason why Wilson's disease has such a high prevalence of fatty lipomas is because zinc levels go down when copper is high, preventing cytokines to be removed in the normal fashion from injuries. It is known that an injury may result in a fatty lipoma. But it doesn't usually happen, particularly in people whose bodies are able to control cytokines; "healthy."

(Another possible factor is low iron, which can happen with high or low copper, can prevent proper healing. Whether this could cause fatty lipomas without cytokines, whether it is contributory, or whether it is irrelevant will be a topic for future study, in the efforts to get a more complete understanding of the total range of causes and contributory factors.)

High copper and low zinc would support the cytokine theory, because cytokine storms happen when someone is low on zinc. Zinc is a copper antagonist, as well as an antagonist of mercury, lead, cadmium, aluminum, lithium, fluoride, and possibly other metals.

In a similar vein, folic acid is a cofactor with zinc in various processes in the body. If one cofactor is in excess to the point that it cannot leave the body or be stored, the other cofactor will be reprioritized from its normal singular duties to join with the excessive cofactor to use it up. An example of this would be people who have coronavirus, those who lose their sense of smell tend to have a lighter case because the body doesn't have so much folic acid that it can't get rid of it normally and allow the zinc to be prioritized to the immune system.

People who thus use the sense of smell this way as a "zinc bank," making up for the fact that there is no zinc storage in the body, tend to have lighter cases of Coronavirus.

Therefore if any of the zinc antagonists or its cofactor are high when a person gets injured, causing zinc to be low, cytokines would not be controlled.

The only reason why certain people would not be simply covered with fatty lipomas would be because the body copes with nutritional deficiencies, insufficiencies or excesses by optimizing the blood as much as possible, causing the blood to be correct and putting the deficiencies into cells that are less important. These intracellular deficiencies would also not show up via serum testing, because the body does not know that there's a doctor out there who, if given the right test result, will help it. In the meantime, this coping mechanism keeps the blood at a better level of zinc, so that fatty lipomas are much rarer on the body than they would be. Otherwise a person with Wilson's disease could have a lipoma everywhere that they had received a bruise on fat.

-----

When you have the right questions, you get the right answers. Having first-hand experience with new lipomas showing up during certain circumstances, I knew what questions to ask. My personal experiences guided me to the wealth of research now available in line, the results of possibly trillions of hours of other people's work. With these right questions, I believe I have come up with some worthwhile answers, by learning from and leaning on all the research that has gone on before me, available via government, medical and scientific websites.

Although I do not have Wilson's disease, I also have other conditions which correlate with it as a result of what the Walsh protocols call copoer overload, including:

  • renal acidosis
  • mania
  • oversalivation
  • trouble swallowing
  • enlarged left ventricle (from decades of iron deficiency)
  • ataxia (to using a walker when taking lithium carbonate, which prevents the body from putting copper into amyloid plaque by alkalizing the brain, leaving slightly more copper free in the body)
  • psoriasis (the body gets rid of folic acid by causing skin overgrowth so that its cofactor, zinc, can be prioritized to getting rid of extra copper)
  • arthralgia (particularly with septra antibiotic)
  • miscarriage
  • diabetes (improved with zinc)
  • bradiacardia (possibly from high norepinephrine induced by low iron, preventing the body to from turning norepinephrine to adrenaline. This has been studied in rats)
  • hyperpigmentation
  • leucopenia (when taking allopurinol)
  • cysts: dermal, subdermal, at the base of a tooth, and excision required for two ganglionic cysts, one at the right wrist (scaphoid radial juncture) and one in the right knee
I personally am covered with hundreds small subcutaneous lipomas, a number of larger ones, and a fist-sized one above my left knee. Copper being a zinc antagonist would result in lower levels of zinc and slower removal of cytokines, causing my large quantity of fatty lipomas.

It would also explain a craving for red meat, because is higher in zinc, but since it also is rich in iron, it would allow iron and copper to join together to be used up by the body via the transitions from one to the next of the catecholamine family of neurotransmitters, ending with adrenaline, causing mania. I have had hypomania from 9 years old, which correlates with copper overload via copper and iron being used up by the body via the neurotransmitter transitions of the catecholamine family, which ends in adrenaline. When my iron is deficient, I get bradycardia, and the mania reduces. This is happened repeatedly once I got the copper iron homemade homeostasis issues which go with fibromyalgia.

When on Depakote, which causes a deficiency of iron, I had a constant low-level anemia. Eventually this and other nutritional deficiencies induced by Depakote, particularly the l-carnitine deficiency (ICD Code E71.43) made me an able to become unable to become manic, causing an overdose of lithium. When I started taking nutritional supplements, my mania came back and I had to go back on the lithium. Considering the neuroprotective effects of lithium, and the damage to my hypothalamus and minor shrinkage to my cerebellum, as well as the left ventricular hypertrophy and increased mental illness from nutritional deficiencies from a mental illness medication, I'm much better with just the lithium and having used the Depakote temporarily as a stabilizer until the lithium took over, which for me is only two weeks.

It all links together.

The problem with diagnosing nutritional deficiencies or excesses is that the body has a large choice of areas to put the excess or deficiency, causing a range of symptoms which will not hit anyone specialty. Therefore the doctors will each have one point of data, which is not enough to make any speculation as to an ultimate cause.

This is why the authors of Acute-Onset Optic Neuropathy in Wilson's Disease describes Wilson's disease as the great masquerader. And this is why it is important that doctors look at the body holistically. Taking a medication for one condition can prioritize nutrients that are being shared among the systems in a mild insufficiency so that the body will place that nutrient in helping a particular system to the detriment of others.

Contrariwise, sometimes it's even a benefit. As of 1970, it has been known that calcium channel blockers can cure certain types of mental illness. As it turns out, further research shows that any of the basic four types of blood pressure medications can either cause or cure mental illness, helping one type but hurting another.

Unfortunately, the doctors who prescribe blood pressure medications do not discuss this with psychiatrists, so that an increase in stress requiring a blood pressure medication could cause new or increased in mental illness which could increase stress. The new increased mental illness would then require medication which might then prioritize nutrients back, or deplete them, causing further health issues rather than fixing them.

Wilson's disease could highlight this problem and allow doctors to thus start working on how to deal with it.

-----

References:

1 Nigri, G., Dente, M., Valabrega, S. et al. Giant inframuscular lipoma disclosed 14 years after a blunt trauma: A case report. J Med Case Reports 2, 318 (2008). https://doi.org/10.1186/1752-1947-2-318

From the above: 

  • 1.Aust MC, Spies M, Kall S, Gohritz A, Boorboor P, Kolokythas P, Vogt PM: Lipomas after blunt soft tissue trauma: are they real? Analysis of 31 cases. Br J Dermatol. 2007, 157 (1): 92-99. 10.1111/j.1365-2133.2007.07970.x.
    CAS Article PubMed Google Scholar 
  • 2.Copcu E: Sport-induced lipoma. Int J Sports Med. 2004, 25 (3): 182-185. 10.1055/s-2003-45254.
    CAS Article PubMed Google Scholar 
  • 3.Copcu E, Sivrioglu NS: Posttraumatic lipoma: analysis of 10 cases and explanation of possible mechanisms. Dermatol Surg. 2003, 29 (3): 215-220. 10.1046/j.1524-4725.2003.29052.x.
    PubMed Google Scholar 
  • 4.Penoff JH: Traumatic lipomas/pseudolipomas. J Trauma. 1982, 22 (1): 63-65.
    CAS Article PubMed Google Scholar 
  • 5.Brooke RI, MacGregor AJ: Traumatic pseudolipoma of the buccal mucosa. Oral Surg Oral Med Oral Pathol. 1969, 28 (2): 223-225. 10.1016/0030-4220(69)90290-4.
    CAS Article PubMed Google Scholar 
  • 6.Lemperle G: Posttraumatic lipoma. Plast Reconstr Surg. 1998, 101 (4): 1159-
    CAS Article PubMed Google Scholar 
  • 7.Signorini M, Campiglio GL: Posttraumatic lipomas: where do they really come from?. Plast Reconstr Surg. 1998, 101 (3): 699-705. 10.1097/00006534-199803000-00017.
    CAS Article PubMed Google Scholar


# Dzieżyc-Jaworska K, Litwin T, Członkowska A. Clinical manifestations of Wilson disease in organs other than the liver and brain. Ann Transl Med 2019;7(Suppl 2):S62. doi: 10.21037/atm.2019.03.30
Cysts,Joint,Cu↪heart!,

# Acute-Onset Optic Neuropathy in Wilson's Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6341316/

# Klaus Johansen, MD; Gunnar Gregersen, MD Glucose Intolerance in Wilson's Disease Normalization After Treatment With Penicillamine Arch Intern Med. 1972;129(4):587-590. doi:10.1001/archinte.1972.00320040063007
https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/579263

Moderate glucose intolerance, hyperresponse of insulin production not suppressed in blood in two siblings with Wilson's disease normalized after treatment for a year, when the liver had returned to normal.




-----
©Deborah Barges Oct 2020 open access
I BUILT MY SITE FOR FREE USING