And it’s NOT vitamin C…
Using this unique combination of 4 supplements in a special way gives men these advantages:
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This natural vitamin fights off viruses
Vitamin D3 is often falsely heralded as a cure‑all, somehow capable of magically fixing nearly any condition.
Yet its antibacterial activity is certain and cannot be discounted.
Yet, even within this smaller realm of battling microbes, vitamin D3 cannot be considered a cure‑all either.
Vitamin D3isn’t so much a broad‑spectrum antibiotic… But it is extremely potent against certain microbial invaders.
You will soon see why this is the case – including proof that vitamin D3is particularly effective against Helicobacter pylori, Mycobacterium tuberculosis, and Borrelia burgdorferi.
(H. pylori infects the digestive system. We know what tuberculosis is. And B. burgdorferi causes Lyme disease.)
Most people seem to view vitamin D3 as having only “nebulous immune‑stimulatory effects.”
But what vitamin D3 actually does is definable, distinct, plain as day, and has little to do with cytokines.
(Cytokines are proteins that are important in cell signaling. Among other things, they are involved in immune response and are markers of inflammation.)
The antibacterial effects of vitamin D3 boil down to just two mechanisms – one well‑known among scientists and the other rather obscure.
Here is the mainstream explanation for how vitamin D3 exerts antibacterial activity (and how sunlight cures tuberculosis):
It stimulates immune cells to produce cathelicidin – an antimicrobial peptide.
This is certainly true and highly relevant.
But what is often overlooked is that D3 exerts direct antimicrobial activity against certain bacterial species.
“Therefore, it can be stated that vitamin D is a bactericidal, bacteriostatic, and bacteriolytic substance in vivo and in vitro.” (Raab, 1946)
Yes, you read that correctly…
Vitamin D3 also works in vitro in a manner completely independent of immune cells, even in concentrations lower than cathelicidin.
(In vitro = in glass. In vivo = in live cells or organisms.)
This fact was proven as far back as 1946, yet it wasn’t until recently that it was rediscovered and further elaborated on:
Although H. pylori causes ulcers and not Lyme disease, and thus may seem irrelevant, this study provides the proof needed to explain the studies which follow.
They discovered that vitamin D3 would completely destroy H. pylori in concentrations as low as 5 μM (micromolars).
But, at the same time, it was totally ineffective against other species: E. coli, S. aureus, P. aeruginosa, K. pneumoniae, P. mirabilis, S. marcescens, and S. enterica.
These other bacteria were not affected by D3 at any concentration.
In addition, this specific effect against H. pylori was more potent with older stocks of vitamin D3.
And this led the researchers to infer that a breakdown product was the active agent.
Upon isolating individual breakdown products, this turned out to be true.
And this was further confirmed by synthesizing one of the breakdown products known as Grundmann’s ketone.
Grundmann’s ketone is simply the upper half of vitamin D3 as it is usually depicted.
This product forms spontaneously through the action of heat and/or light, and it completely inhibits H. pylori at concentrations of 3 μM.
They also demonstrated that Grundmann’s ketone is non‑toxic to human cells – and that it has no vitamin-D3-like hormonal activity.
Grundmann’s ketone (abbreviated as VDP1 in this study) was even more powerful than the antibiotics amoxicillin and kanamycin:
“[…] VDP1 conferred a more rapid bactericidal action against H. pylori than the other two antibiotics.”
All three forms of vitamin D3 – cholecalciferol, calcidiol, calcitriol – were equally effective.
This might imply that vitamin D2 could have a similar bactericidal effect…
And that could be preferred in certain instances due to its lower calcemic (excess calcium in the blood) potency.
In fact, vitamin D2 was actually proven effective over a half‑century ago.
Based on the remarkable success of sunlight in eliminating tuberculosis, studies were undertaken to unravel the reasons underlying this curative effect:
There had been numerous studies up to this point showing that injections of either vitamin D2 or D3 can eliminate M. tuberculosis in living people.
But this was one of the first to demonstrate its in vitro effects.
They used vitamin D2 in this study and found that it was capable of completely inhibiting the growth of M. tuberculosis at a concentration of 50 units per cubic centimeter.
“It was shown that tubercle bacilli do not grow on media to which vitamin D in water-soluble form…50 units per cc. of the medium had been added.”
If these “units” of vitamin D2 he speaks of are equivalent to our modern system of international units (I.U.), this would correspond to a concentration of 3.2 μM.
This is practically identical to the amount found to inhibit H. pylori.
And, like the H. pylori study above, this one found that only certain bacterial species were particularly susceptible to vitamin D.
M. tuberculosis was 6 to 30 times more susceptible to vitamin D2 than all other bacterial strains tested:
“In agar plates, the inhibition of growth of proteus, B. aerogenes, and staphylococci was noticeable in 24 hours… However, it is interesting to compare the amount of vitamin D necessary, which was from 6 times to 30 times as much as tubercle bacilli in their culture media.”
So now we now know of two bacterial species that are particularly susceptible to vitamin D:
- Helicobacter pylori (stomach ulcers and other gut infections)
- Mycobacterium tuberculosis (tuberculosis)
Conversely, through these studies, our list of those less affected by vitamin D has expanded:
- Escherichia coli (E. coli)
- Staphylococcus aureus (staph infections)
- Pseudomonas aeruginosa (includes hospital-acquired infections such as ventilator-associated pneumonia and sepsis)
- Klebsiella pneumoniae (e.g. pneumonia, meningitis, sepsis)
- Proteus mirabilis (e.g. catheter-associated urinary tract infections)
- Serratia marcescens (hospital-acquired infections such urinary tract infections, wound infections)
- Salmonella enterica (salmonella)
- Klebsiella aerogenes (causes opportunistic infections)
- Streptococcus spp. (e.g. pink eye, meningitis, bacterial pneumonia, “’flesh-eating” infections)
Yet there is evidence that at least one more bacterial species is particularly susceptible to vitamin D, and that is Borrelia burgdorferi.
That’s the spirochete (spiral-shaped bacteria) that causes Lyme disease.
These Californian researchers tested 15 natural compounds against two Borrelia species: B. burgdorferi and B. garinii.
Incidentally, this study was co‑authored by Dr. Matthias Rath who worked with Linus Pauling concerning vitamin C in cardiovascular disease.
And, of the natural compounds tested in this study, vitamin D3 had the greatest anti‑spirochetal activity by far:
Vitamin D3 greatly surpassed all other compounds tested, including the antibiotic doxycycline – by a minimum margin of 10,000‑fold.
And this effect is certainly not a fluke, an outlier value, or a typographical error…
Because the very same concentration of vitamin D3 was found to be effective in a follow‑up study (Goc, 2016).
Even more amazing than its relative efficacy is the minute concentrations needed to inhibit B. burgdorferi.
B. burgdorferi is inhibited by vitamin D3 in the nanomolar range (1.3 nM), making this bacteria the most sensitive to vitamin D3 thus far examined.
Could this be why the white‑footed mouse, a nocturnal animal, is the only natural reservoir of B. burgdorferi?
As a nocturnal species, these mice would receive very little sunlight…
So it would make sense that they would therefore maintain low serum vitamin D concentrations.
This idea actually has more evidence to support it:
It has been shown that blood serum from most animals completely destroys B. burgdorferi…
Yet blood serum from the white‑footed mouse is completely ineffective at destroying the spirochete.
This study also confirmed the contention that, contrary to popular belief, deer are not natural reservoirs of B. burgdorferi:
Serum from deer was completely lytic to the spirochetes (i.e. it killed them) within hours.
“Deer and lizard sera were completely borreliacidal for B. burgdorferi, B. bissettii CO-501, and B. bissettii DN127… Rabbit serum was partially lytic for all three strains of Borrelia… Mouse serum was nonlytic for all three Borrelia strains.”
In fact, it’s been shown by other researchers that ticks feeding on deer eventually become spirochete‑free (Roome, 2016).
Ticks collected from deer tested positive for Borrelia only rarely.
But ticks found in the weeds – collected by “dragging” – were found infected at much higher rates (37 to 56%):
It has also been demonstrated by others that white‑footed mice do in fact create antibodies against B. burgdorferi (Schwan, 1989).
So it’s not just that their bodies are simply ignoring it.
So why can’t white‑footed mice kill the spirochetes like most other mammals, despite raising antibodies against them?
The answer could lie in vitamin D3, a molecule barely present in nocturnal animals.
“Persistent spirochetal infection in some mice, in spite of a strong and diverse antibody response, deserves further investigation.” (Schwan, 1989)
In the study above, heat treatment abolished the bactericidal activity of deer serum – thus ruling out activity of Grundmann’s ketone as a factor.
However, this does not discount the idea of D3 being the prime actor here because vitamin D3 also transcribes for cathelicidin, an antimicrobial peptide.
In another study, the active form of cathelicidin (called LL‑37) was the most effective antimicrobial peptide – among seven tested – against Borrelia garinii (another type of Borrelia that causes Lyme disease):
In the US, Lyme disease is reported predominantly in Northern states – areas of relative vitamin D3 deficiency:
So, just as sunshine or vitamin D3 supplementation can make a person tuberculosis‑proof, they may also make them Borrelia‑proof.
—-Important Message For Men Who Want to Be Bigger Down There—-
How to boost blood flow to boost size
Blood flow is the key to getting large and engorged “down there.”
So if there’s not enough blood flowing to a man’s penile member, it will shrink and look smaller than it really is…
But the second you get lots of hot, pumping, oxygen-rich blood flowing to your member again, the bigger you’ll look…
The penile chambers will expand with fresh blood, and this will make you look bigger and more engorged down there almost instantly.