Fish oils and their DHA content impair cellular immunity, specifically your macrophages and
their interferon-gamma production. It's not a good idea to take omega-3 oils if you have TB
or other bacterial/viral/parasitic infection.
"However, the same anti-inflammatory properties which are so beneficial in
chronic inflammatory diseases may be detrimental in the context of anti-microbial
immunity. Indeed, n-3 PUFA feeding increases mouse susceptibility to intracellular
pathogens, such as Listeria monocytogenes, Salmonella typhimurium and
Guinea pigs infected with virulent M. tuberculosis fed with n-3 PUFA, and transgenic fat-1
mice with endogenous enrichment of n-3 PUFA, showed increased bacterial loads and pronounced
progression of the disease . These experimental findings suggest that increased tissue levels of
n-3 PUFA can impair resistance to TB. "
" ..... macrophage activation is indispensable for clearance of mycobacteria and
other intracellular microbial pathogens. Macrophage activation leads to induction
of a variety of cellular processes and allows control of intracellular pathogens in
a more effective way. n-3 PUFA decrease macrophage activation in response
to LPS, IFNγ, or TLR ligands. "
Deactivating effects of n-3 PUFA on macrophage activation
and antimicrobial responses
" Macrophages are both host and effector cells for M. tuberculosis, being responsible
for mycobacterial killing via enzymatic degradation within mature phagolysosomes
and through generation of oxygen and nitrogen reactive species. M. tuberculosis is able
to evade the macrophage response and the effectiveness of those antimycobacterial
mechanisms depends on an appropriate level of macrophage activation [Deretic et al.,
1997; Vergne et al., 2004. IFNγ activates macrophage maturation [Via et al., 1998],
inducing upregulation of proinflammatory cytokines and surface markers. However,
n-3 PUFA have been found to impair IFNγ -induced activation, thereby reducing the
ability to kill some pathogens and to stimulate an acquired immune response.
Different processes important for killing activity are affected by DHA, including the respiratory burst,
chemotaxis, antigen presentation, the expression of adhesion molecules and MHC class II and class I.
It has been also established that DHA-treated cells produce less pro-inflammatory eicosanoids and cytokines,
such as IL-1β, IL-12p70 and TNFα, which are known to be associated with a protective response to TB.
Furthermore, lipids have been found to influence phagolysosome maturation which is critical for
mycobacterial clearance by macrophages. Arachidonic acid induced actin assembly,acidification and
lysosome fusion in phagosomes from Mtb-infected macrophages, leading to more effective mycobacterial
control. In contrast, DHA inhibited actin assembly and favored mycobacterial survival. This inhibitory effect
on phagosome maturation might also be mediated by modification of the endosomal membrane lipid composition.
Together, these studies suggest that n-3 PUFA could impair host resistance to Mtb infection by
suppressing macrophage activation and killing capacity. "
Incorporation of a Dietary Omega 3 Fatty Acid Impairs Murine Macrophage
Responses to Mycobacterium tuberculosis
" Beside their health benefits, dietary omega 3 polyunsaturated fatty acids (n-3 PUFA)
might impair host resistance to Mycobacterium tuberculosis (Mtb) by creating an
immunosuppressive environment. We hypothesized that incorporation of n-3 PUFA
suppresses activation of macrophage antimycobacterial responses and favors bacterial
growth, in part, by modulating the IFNγ-mediated signaling pathway. "
" The fatty acid composition of macrophage membranes was modified significantly by
DHA treatment. DHA-treated macrophages were less effective in controlling intracellular
mycobacteria and showed impaired oxidative metabolism and reduced phagolysosome
maturation. Incorporation of DHA resulted in defective macrophage activation, as
characterized by reduced production of pro-inflammatory cytokines (TNF alpha, IL-6 and
MCP-1), and lower expression of co-stimulatory molecules (CD40 and CD86). DHA
treatment impaired STAT1 phosphorylation and colocalization of the IFN gamma receptor with
lipid rafts, without affecting surface expression of IFN gamma receptor. "
" Macrophages are both host cells for Mtb and effector cells for host resistance, being
responsible for mycobacterial killing. The effectiveness of the macrophage
antimycobacterial activity depends on an appropriate level of cell activation. IFN gamma
activates macrophage maturation, inducing upregulation of proinflammatory
cytokines and surface markers. However, n-3 PUFA have been found to impair
IFN gamma-induced activation thereby reducing the ability to kill some pathogens
and to stimulate an acquired immune response. Different processes important for killing
activity are affected by DHA, including the respiratory burst, chemotaxis, antigen
presentation, the expression of adhesion molecules and major histocompatibility
complex (MHC). DHA-treated cells also produce less proinflammatory eicosanoids
and cytokines which are important for a protective response against TB. Furthermore,
lipids can influence phagolysosome maturation and endosomal membrane lipid
composition, which is critical for mycobacterial clearance. "
" Furthermore, DHA significantly affected the early events of cell signaling in
IFN gamma-treated macrophages which may explain, in part, the negative effects of
DHA on macrophage resistance to Mtb. "
Dietary Polyunsaturated Fatty Acids Modulate Resistance to
Mycobacterium tuberculosis in Guinea Pigs
" (n-3) Fatty acid-fed guinea pigs had more bacteria in the lungs compared with (n-6)
fatty acid-fed guinea pigs at 3 and 6 wk postinfection. These data document the
immunomodulatory effects of (n-3) fatty acid consumption in the context of
tuberculosis resistance. The loss of antigen-specific T-cell functions in addition
to impaired resistance to mycobacterial disease suggests a susceptible
phenotype in (n-3) fatty acid-fed guinea pigs. "
" Evidence in support of this hypothesis comes from epidemiological studies of Greenlanders and Alaskan Eskimos, who despite consuming diets rich in fish oil (FO)
containing (n-3) fatty acids, exhibit an unusually low incidence of cardiovascular and
other inflammatory diseases but an unusually high frequency of TB infection. Further
evidence consistent with these epidemiological observations is provided by
experimental data from (n-3) PUFA-fed guinea pigs infected via the i.m. route with
virulent M. tuberculosis. Pronounced progression of disease and higher bacterial counts
in the spleen were observed in (n-3) PUFA-fed guinea pigs compared with guinea pigs
consuming diets enriched in SFA or (n-6) PUFA. Increased susceptibility to other
intracellular pathogens, including Listeria and Salmonella, in (n-3) PUFA-fed animals
has also been reported. "
" .... the disease was stabilised in 18% of the patients given cod liver oil, compared with
only 6% of those in the control group. Deterioration or death occurred in 33% of
patients given standard treatment alone, but in only 19% of those given cod liver oil,
a reduction of 14%. "
" The 542 inpatients with consumption treated with cod liver oil, were given a dose of
1 drachm (3.6 ml) three times a day, gradually increased, in some few cases up to
1.5 ozs (42 ml) per dose. "
" It was observed that one of the most striking effects of the use of cod liver oil is an
increase in the patient’s weight. A gain in weight occurred in 70%, a loss in only 21%
and in 9% the weight remained stationary. "
" Professor Green says that some children are still given cod liver oil today and
perhaps this relates back to the late 19th and early 20th centuries when cod liver oil
was widely used to treat and prevent tuberculosis. "
" He says: “A role for vitamin D in combating tuberculosis gives a rational basis for
sunshine therapy, which was widely practised for patients in sanatoriums before
chemotherapy became available, as vitamin D is synthesised in the skin when
exposed to the sun. Patients were put out on their beds to lie in the sun in summer
and winter, and many were sent to Switzerland and other sunny countries for
treatment.” He adds that today many patients who develop TB in the UK are found
to be Vitamin D deficient. "
Environmental factors in Tiny Tim's near-fatal illness.
" Dickens was familiar with both rickets and TB and wrote about cod liver oil as a
possible cure for rickets and scrofula. Improved vitamin D status can result in
enhanced macrophage synthesis of 1,25-dihydroxyvitamin D, which increases
the synthesis of the antimicrobial peptide cathelicidin. This component of the
innate immune system has strong killing properties for Mycobacterium
tuberculosis. The combination of rickets and TB represent a crippling condition
that could be reversed by improved vitamin D status. "
Inhibition by retinoic acid of multiplication of virulent tubercle bacilli
in cultured human macrophages
" These results suggest that RA (vitamin A), like vitamin D, may have some
immunoprotective role against human tuberculosis, as historically intimated
by the regular use of vitamin A- and D-rich cod liver oil for the treatment of
tuberculosis before the introduction of modern chemotherapy. "