Hemochromatosis and Autoimmune Conditions


FOTCM Member
Laura said:
A year went by, the KD came along, and naturally she went on that. At first, things went well, but then, bizarrely, everything positive started to reverse and a whole host of symptoms came to the fore. So, off to the endocrinologist who ordered about every test in the book including scans. The test results showed very high ferratin levels, high (but not alarming) hematocrit, higher than should be glucose, low vitamind D again.


So I'll be going to give blood myself. One of the things noted in all the research I've been doing is that the individual with this condition feels better after giving blood - they get their energy back, the head clears, etc. So we'll see if it has that effect on me.

My hematocrit is tested each week since I give plasma each week. I have noticed over the years that the level of my hematocrit was always normal if not sometimes a bit low but since the low carbs high fat / paleo / keto / diet the level has increased. And in the last few months, I was approaching a level that not only I did not like but that it could be dangerous for my health. The nurse where I give plasma asked even me if I was eating nails ! :(

So I had to do something to reduce it.

Then in the last month, I did more physical exercises ( hiking, skate skiing, Cross-country skiing), drink more water and kept giving plasma. When I was tested Monday morning, my hematocrit was back to normal. :thup:



FOTCM Member
Ya'll please don't bother with dietary suggestions. Most of them are useless. The best way to reduce the iron is just to go and decant some medically. Then you can eat pretty much what you want. The amount of iron you save by dietary strategies just isn't significant.


FOTCM Member
Psyche, one of the papers I read - of the bunch I've been uploading to my brain - mentioned something about Raynaud's syndrome being related. Can you find anything on that for Lisa Guliani.

I swear, I think everybody who is fit enough ought to go and donate a pint of blood just to see how it makes them feel in the days after. And ask for regular ferritin checks if they can do so.

I'll be decanting a pint asap.


FOTCM Member
Laura said:
Psyche, one of the papers I read - of the bunch I've been uploading to my brain - mentioned something about Raynaud's syndrome being related. Can you find anything on that for Lisa Guliani.

I received this paper and it made me think of Lisa. There is lupus in her family so she could have a spectrum of lupus. The infection part got my attention too. Other than the viral part, it talks about toxoplasmosis. There is also some correlation with solvents (paint stuff, etc), estrogen mimicking chemicals (pesticides, etc). The smoking part is total nonsense, it is amazing they didn't thought of self-medication. Anyhow, here it is FWIW:

Lupus (2012) 21, 241–250.

Environment and lupus-related diseases

Clinical manifestations of lupus are encountered in a variety of disease entities, including
isolated cutaneous lupus, undifferentiated connective tissue disease, mixed connective tissue
, drug-induced lupus, overlap syndrome, and systemic lupus erythematosus (SLE).
While each entity has been recognized as a specific disease with its own diverse clinical and
serological pattern, one could argue that many findings are common. Could it be that all of
these entities actually represent a spectrum of one disease? Could it be that rather than the
genetic predisposition and hence controlled factors that govern this spectrum of diseases, that
environmental factors associated with SLE could also play a role in the different entities of this
spectrum? The traditional environmental triggers in SLE include sunlight and ultraviolet (UV)
light, infections, smoking, and medications including biologics such as tumor necrosis factor
alpha (TNF-a) blockers. In this review, we update and further substantiate these traditional
factors in the various lupus-related syndromes. We will also discuss the association with vaccine
exposure, industrial estrogens, and other factors. Lupus (2012) 21, 241–250.


Lupus erythematosus is a spectrum of diseases
characterized by diverse clinical and serological
manifestations. Multi-faceted triggers may play a
role. The genetic pattern is complex and not yet
entirely deciphered, and it is probable that exposure
to various environmental agents can determine
which lupus syndrome in the spectrum will develop.

Furthermore, among patients with systemic lupus
erythematosus (SLE), the clinical subset, disease
activity and severity may be governed by genetics
and environmental load. The traditional environmental
factors known to influence the development
of lupus in the genetically prone individual are
exposure to sunlight and ultraviolet (UV) light,
infections, and medications including biologics
such as tumor necrosis factor alpha (TNF-a)
blockers.1,2 [...]

The spectrum of lupus

The lupus-related disease spectrum includes organ specific
disease, i.e. cutaneous lupus, undifferentiated
connective tissue disease (UCTD), mixed
connective tissue disease (MCTD) with specific
manifestations of lupus but of other autoimmune
diseases as well, drug-induced lupus, overlap
syndrome – for example SLE and antiphospholipid
syndrome (APS) – and SLE, the classic multisystemic

[skipped cutaneous and drug induced lupus, read it in the attached document]

Mixed connective tissue disease

MCTD, a discrete entity, is usually a benign syndrome
characterized by specific features of autoimmune
diseases: SLE, systemic sclerosis (SyS), RA [Rheumatoid Arthritis],
and myositis, in the restricted presence of elevated
titers of antibodies to RNP. This is an example
where only one antibody is exclusively required
for the basis of diagnosis. Features reported to be
characteristic of MCTD, occurring more commonly
than, for example, in typical SLE, include severe
Raynaud’s phenomenon, an erosive arthritis
multiple subcutaneous nodules in the peri-tendinous
regions of the forearms and hands, juxta-articular
calcinosis and pulmonary hypertension.25

A prominent histopathologic feature of MCTD
is a widespread proliferative vasculopathy characterized
by intimal and medial proliferation which
results in narrowing of the lumen of small arteries

and larger vessels such as the aorta, coronary, pulmonary
and renal arteries. In addition, the titers of
antibodies to U1RNP are generally very high, usually
much higher than in SLE sera. It is reported
that MCTD is most closely correlated with the
presence of IgG antibodies to the 70 kDa and A
proteins and predominantly IgM antibodies to
the B’B peptides of the Sm system.25 There is
some serological evidence that the autoimmune
response to MCTD is distinctive from that in
SLE and other systemic rheumatic diseases. For
example, epitope mapping studies to determine
the fine specificity of antibodies to U1RNP have
shown differences between MCTD and lupus. An
important observation was that antibody reactivity
to a particular peptide on the A protein was found
in 94% of MCTD patients compared with 19% of
patients with SLE. Similarly, the specific epitope
recognition of a different autoantigen, hnRNP-A2
(or RA33) was also distinctive in MCTD. Amongst
207 patients fulfilling the American College of
Rheumatology (ACR) criteria for SLE followed
prospectively, Raynaud’s phenomenon and myositis
were found to be prominent features in
anti-U1RNP-positive patients
, with 55% of this
serological group fulfilling the clinical components
of MCTD criteria compared with only 3% of the
152 lupus patients without these antibodies.25,26
Reports describe MCTD patients with higher circulating
TNF-a levels than in patients with SLE. The
development of additional SLE- or SyS-associated
autoantibodies during the course of MCTD is very

In a retrospective observation over 8 years, some
MCTD patients went on to develop SLE or SyS. In
this report it was unclear if these patients really had
MCTD or evolving lupus with high titers of antibodies
to RNP.27

Although not pathognomonic for any of the diseases,
the antibody response against hnRNP-A2
(RA33) distinguishes MCTD patients from SLE
and RA patients by virtue of the difference in epitope

MCTD has a distinct genetic profile associated
with the HLA-DR4, -DR1, and (less prominently) -
molecules which is not identical to those
that are found most commonly in SLE, SyS, or
polymyositis/dermatomyositis – the three MCTDrelevant
diseases. Hence, it is reasonable to postulate
that MCTD falls within the spectrum of
lupus-related diseases

In a literature search for environmental factors
associated with MCTD, surprisingly, no relevant
articles were found. Further investigation into
potential environmental triggers including drugs,
sun exposure, occupational risks, or hormonal
exposure is warranted in these patients.

Undifferentiated connective tissue disease

UCTDs are defined by a limited set of clinical and
serologic features that do not meet all the criteria
for connective tissue diseases (CTDs)
as opposed to
MCTD which has set clinical and serological characteristics
and fulfil respective diagnostic criteria.

Cumulative evidence suggests that some of these
patients will remain in the UCTD subset while
others will develop well-defined autoimmune diseases
over time.
A subset of patients with UCTD
have a mild type of lupus and develop clinical
manifestations suggesting lupus, but do not upon
presentation, fulfil four of 11 ACR criteria for the
definite diagnosis of SLE
. It is known that autoantibodies
circulate in the blood years before the
onset of clinical disease.28 Possibly, in some individuals,
the UCTD lupus subset represents the gradual
onset of disease instead of a full-blown pattern.
Some patients usually have elevated titers to antidsDNA
antibodies upon presentation, and some
rheumatologists even initiate therapy at this point.
The majority of patients with SLE will develop the
classical disease usually within 2 years.
Compared with SLE, evidence for environmental
triggers of UCTD are sparse. Plasma levels of
25(OH)D3 in 161 UCTD patients were significantly
lower compared with controls. The presence of
dermatological symptoms (photosensitivity, erythema,
and chronic discoid rash) and pleuritis was
associated with low levels of vitamin D. During the
average follow-up period of 2.3 years, 21.7% of
UCTD patients developed well-established CTD.
Patients who progressed into CTDs had lower
vitamin D levels than those who remained in the
UCTD stage. These results suggest that vitamin
D deficiency in patients with UCTD may play a
role in the subsequent progression into well-defined

Sporadic reports suggest that solvents are associated
with UCTD among other autoimmune
diseases. Yet it is difficult to establish a true relevance
due to lack of replication, an inability to
specify which solvents convey risk, and an absence
of increasing risk with increasing exposure.30 For
example, in one study, detailed information on
solvent exposure was ascertained from 205 women
who had at least two autoimmune related symptoms
but did not fulfil ACR criteria for defined
disease and were diagnosed between 1980 and
1992, and compared with 2095 population-based
controls. Among 16 self-reported occupational
activities with potential solvent exposure, furniture
refinishing, perfume, cosmetic, or drug manufacturing,
rubber product manufacturing, work in a
medical diagnostic or pathology laboratory, and
painting or paint manufacturing were significantly
associated with UCTD
. After expert review of selfreported
exposure to 10 specific solvents, paint
thinners or removers and mineral spirits were associated
with UCTD.31

Overlap syndromes – SLE and APS

The most common overlap syndrome in lupus related
diseases is SLE–APS. Some 40% of SLE
patients develop secondary APS with clinical
manifestations of recurrent venous and arterial
and/or recurrent fetal loss in the setting of
autoantibodies to cardiolipin, beta-2-glycoprotein
I, or lupus anticoagulant. The presence of SLE–
APS overlap can skew clinical lupus manifestations
and be associated with focal CNS findings
including stroke and seizures or cardiac disease
(Libman–Sacks endocarditis). As in SLE, circulating
antibodies are encountered prior to clinical disease.
Distinct polymorphisms of common genetic
factors have been associated with SLE and primary
APS, supporting the notion that these entities are
indeed variants within a continuum of the same
disease.32 The support for the influence of infectious
triggers in APS is vast and beyond the scope
of this chapter (and is reviewed elsewhere).33,34
In a recent study, 98 patients with APS were
screened for antibodies directed to several infectious
agents. The main finding in this study was
the significantly higher prevalence of IgM antibodies
to toxoplasma and rubella.
This novel finding
suggests that these infections might be associated
with APS. A current infection with certain agents,
i.e. toxoplasma and rubella, might either be related
to the pathogenesis of APS or alternatively to its
35 We found that rubella antibodies
may be associated with neuropsychiatric lupus while
Epstein-Barr virus (EBV) exposure does not correlate
with APS.36,37

Mounting evidence suggests that SLE and APS
are yet another face to the spectrum of lupusrelated
disorders.38–41 While some common environmental
triggers are associated with increased
thrombophilia (smoking, estrogens), other environmental
triggers such as hydrazines, solvents, and
pesticides were associated with an increase risk of
developing SLE. In the Women’s Health Initiative
Observational Study, women who had exposure to
pesticides had a higher risk of developing SLE and
;42 however, this result was contradicted in
some studies regarding pesticides.38 Individuals
exposed to solvents (e.g. nail polish, metal cleaning
products) have a higher risk of developing SLE.

Clinical diversity of SLE

SLE is a multi-systemic autoimmune disease with
diverse patterns of clinical and serological manifestations.
SLE is characterized by autoantibody production.
44 At least 20 different autoantibodies have been
reported with neuropsychiatric involvement that
target brain-specific antigens and systemic antigens.40

Are clinical subsets influenced by exposure to
various environmental factors? Can environmental
triggers further influence the spectrum or pattern of
disease? Can exposure to infections influence the
clinical pattern of lupus disease?

SLE and infections/vaccines as triggers of disease

We have investigated the association of viral infections
and SLE. In previous studies, we compared
the titers of antibodies to infectious agents with
lupus clinical manifestations. The sera of 260 individuals
(120 patients with SLE and 140 geographic
controls) were evaluated for the titers of EBV,
cytomegalovirus (CMV), toxoplasma, rubella and
syphilis antibodies. Correlation analysis indicated
that rubella IgM antibody titers were marginally
positively associated with neuropsychiatric lupus
(NPSLE) manifested as psychosis.36
Exposure to EBV infection predicted a disease
phenotype of mild SLE disease with cutaneous
and joint manifestations and elevated titers of
anti-Ro antibodies. No evidence of severe disease
demonstrated as renal or neuropsychiatric involvement
was associated with prior EBV exposure.
These studies suggest that in the genetically prone
individual, particular infectious exposure may skew
the patient toward specific organ involvement, or
may affect disease severity

Furthermore, exposure to certain vaccines may
elicit an autoimmune effect in genetically prone
. For example, SLE has been diagnosed
in patients following vaccination with hepatitis B
virus and influenza.
45 Following tetanus toxoid,
influenza vaccines and polio vaccine there were
anecdotal reports of autoantibody production and
even RA
.46 In a study of 173 patients with SLE,
cervical samples were collected demonstrating
threefold findings of HPV infection in these
patients. This was associated with the immunosuppressive
therapy given to the patients,47 suggesting
that SLE patients should be vaccinated against
HPV. It should be noted that in sporadic cases
SLE developed following the HPV vaccine.45

SLE and hormonal triggers

There is no doubt that estrogen plays a direct role
in the immune system, as demonstrated in numerous
experimental lupus models. Environmental
sources of estrogen including oral contraceptives,
hormonal replacement therapy, preparation for
in-vitro fertilization, preparation for sex reassignment
surgery, estrogens found in plastic bottles,
pesticides, alternative medicine (phytogens) and
probably other sources, may play an added role
in the development or exacerbation of lupus
In addition, blockade of estrogen effects with selective
estrogen receptor modulators may have a beneficial
effect on disease activity in lupus-prone

While it has been traditionally thought that
exogenous estrogens in the form of oral contraceptives
may play a role in the development of lupus,
recent studies have shown a less dramatic effect and
the evidence to date is mixed, mostly regarding
a higher risk of developing thrombosis in menopausal
patients with SLE who are treated with
hormonal replacement.50 Global disease activity,
maximum SLEDAI score, incidence of flares, time
to first flare, and incidence of adverse events were
similar among women with SLE, irrespective of
the type of contraceptive utilized. Therapy with
estrogen as hormone replacement therapy for
post-menopausal women is predominantly related
to mild lupus flares.51

Recently, there has been much controversy
about the presence of estrogens in industry.
Phthalates, natural compounds found in mushrooms,
have an estrogenic effect. Xenoestrogens, a
group of synthetic compounds that mimic estrogen,
could affect the endocrine system and stimulate the
immune system.5
In one study, SLE-prone mice
exposed chronically to xenoestrogens such as
DDT showed accelerated development of albuminuria.
49,52,53 More investigation is warranted on the
impact of these compounds on the immune system
and the development or even the exacerbation of
SLE. The effects of sex hormones are well established
in SLE, but have not been described in other
lupus-related syndromes. In anecdotal studies,
decreased androgen levels had an immunosuppressive
effect, causing dysregulation of the immune
system which in turn may lead to non-specific autoimmune

SLE and UV triggers

Photosensitivity is a known trigger for systemic
disease. Recent evidence points to the possible
detrimental effect of exposure to artificial light.

UVA2 and UVB can exacerbate skin disease in
patients with lupus, while UVA1 may be protective.
Halogen lamps emit significant levels of UV radiation
and should be covered with glass prior to use.
Incandescent bulbs emit low-dose UV radiation.
Fluorescent bulbs emit varying levels of UV radiation,
and patients should strive to use bulbs with
the lowest irradiance
. UV exposure in doses similar
to those emitted from compact fluorescent light
bulbs induces DNA damage, tumor formation,
and erythema.55 In one study, patients with SLE
had an increased risk for blisters and/or rash after
2 h exposure to sunlight.43

Additional studies must be performed to determine
the lowest dose capable of causing damage in
photosensitive patients.55 The exacerbation of SLE
following exposure to cosmetic sun-tanning apparatus
has been reported.56 UVB not only induces
apoptosis, but also plays a role in the recruitment
and activation of opsonins including CRP and
MBL so as to facilitate the clearance of apoptotic
cells. The dose of UVB determines the rate of
apoptosis, the degree of autoantigen translocation
to the cell surface, and the level of cytokine

Paradoxically, the persistent abstention from sun
exposure in the general population has lead to
impaired immune system function related to vitamin
D deficiency.58 There is growing interest in this
topic, with many recent studies on the contribution
of vitamin D deficiency in SLE.59–63 Vitamin D
deficiency skews the immunologic response towards
loss of tolerance which is reversible. Most crosssectional
studies show an inverse relationship
between levels of vitamin D and disease activity.59
Data from a population-based cohort study of 123
recently diagnosed SLE patients found a trend
toward lower 25(OH)-D levels in cases compared
with controls, which was statistically significant in
Caucasians. Overall, 67% of the subjects were vitamin
D deficient, with mean levels significantly
lower among African Americans compared with
Caucasians. Critically low vitamin D levels (<
10 ng/ml) were found in 22 of the patients with
SLE, with the presence of renal disease being the
strongest predictor followed by photosensitivity.59
In a recent study of 378 patients with SLE an
inverse correlation was demonstrated between vitamin
D levels and disease activity.63 Vitamin D is
implicated in many biologic mechanisms unrelated
to calcium homeostasis. Of interest are the downregulating
mechanisms of interaction with the
adaptive and innate immunity through the regulation
of B cells, T cells, dendritic cells, and toll-like

SLE and occupational environmental triggers

Other potentially hazardous environmental agents
that may play a role in the development of lupus
include xenobiotic organic and inorganic compounds,
silica dust, silicone implants, organic
solvents, petroleum, and related by-products.
An example is hydrazine, a compound used in
agricultures and industry, synthesis of plastics,
anti-corrosives, rubber products, herbicides, photographic
supplies, preservatives, textiles, dyes, pharmaceuticals,
and in tobacco.5,64,65

Although silicone implants for augmentation
mammoplasty were reported in some lupus-related
cases, no causative effect was determined.66,67


In conclusion, exposure to various environmental
agents may determine which lupus-related
syndrome (cutaneous lupus, drug-induced lupus,
MCTD, UCTD, overlap syndrome, or SLE) will
develop. Cutaneous lupus is elicited by exposure
to UV light, drugs, exogenous estrogens, and smoking.
Over 80 drugs are implicated in drug-induced
lupus manifested by mild disease with elevated
titers of anti-histone antibodies. Exposure to biologics,
such as TNF-a blockers, leads to the development
of systemic severe disease with expected
elevated titers of anti-dsDNA antibodies. MCTD
is a distinct entity with features of lupus, and environmental
causes have not been reported. UCTD
may originate with initial findings of lupus and
hence may be influenced by environmental exposure,
as in the case of vitamin D deficiency and
possible occupational related agents. Infectious
agents will influence the clinical manifestations of
SLE. For example, exposure to rubella may be
involved in the development of neuropsychiatric
lupus, where exposure to EBV may be associated
with skin and joint involvement. Other recently
investigated triggers include exogenous estrogens,
as found in oral contraceptives, hormone replacement
therapy, sex reassignment surgery, phthalates
(plastics), and others. Deficient levels of vitamin D
and smoking have been linked to the development
of lupus. Environmental triggering factors of the
lupus spectrum are summarized in Table 1.
The extent of environmental factors on the
development of other lupus-related diseases is yet
to be discovered. Could it be that an environmental
load is responsible for systemic disease? While environmental
factors have been well-defined in cutaneous
lupus and SLE, information is lacking
regarding MCTD and overlap syndromes.


FOTCM Member
[skipped cutaneous and drug induced lupus, read it in the attached document]

Which I forgot to attach! Here it is now.


  • lupus related diseases.pdf
    111.5 KB · Views: 7


FOTCM Member
Mercola's take on excess or iron (he starts talking about it at about 2.40 minutes after the video starts)

He recommends donating blood regularly as well.

Then, there is this series of videos. I've only watched two, but found them to be really interesting.

Mrs. Peel

The Living Force
FOTCM Member
Tea and Coffee
According to the National Institutes of Health, teas like black tea and pekoe tea, have substances that bind to iron in the body, making the body unable to use the iron. Polyphenols, found in coffee, can also bind to iron, according to Dr. Srimathi Kannan of the American Dietetic Association. He states that black tea has the strongest ability to bind iron of all beverages, followed by coffee and then herbal teas like chamomile tea.

I'm trying to read all this info but it's really making my eyes hurt, so is eating something that binds to iron good or bad? If it means you won't absorb it and you have high iron, that's good? Or conversely, if you are low in iron, and you eat foods that bind to it, you don't absorb it and can become anemic, and that's bad, right?

My iron in a blood test of March 2012 was only something like 56, and came out as low, so I started taking a liquid iron supplement, and when I had more bloodwork in the fall, the doc asked me if I was taking iron cause it must have went up, and she said to quit taking it but cook with an iron skillet. I have no clue what it is now, but am getting bloodwork towards the end of March so I'll see where I am now. I was anemic as a kid.


FOTCM Member
Laura said:
A year went by, the KD came along, and naturally she went on that. At first, things went well, but then, bizarrely, everything positive started to reverse and a whole host of symptoms came to the fore.

Indeed. And there might be a clue here:

Celiac disease is linked to a very rare genetic disease of iron overload, called hemochromatosis. (Symptoms include chronic fatigue and abdominal pain, among others.) People with celiac disease who also have hemochromatosis may not know it because the malabsorption of celiac protects them from accumulating too much iron—until they go gluten free. As they change their diet, their intestines heal and their iron levels can rise dangerously. Serum ferritin is the best test to screen for iron overload.

And about the same is said here: http://www.livestrong.com/article/550942-gluten-intolerance-skin-hives-hemochromatosis/

If the what the above quote says is true, then no wonder she started developing all those symptoms after we went gluten free! On the other hand, it might be a blessing, since it can also mean that her gut is much healed, which can help enormously once she starts doing the bleeding regularly.

This makes me think that it is very likely that some of the symptoms reported by members of the forum when they started cutting off gluten might also be the related, indeed.

I'm too tired to keep digging right now, but hopefully some of you will find more info on this, and studies. I've also read that there are several skin conditions associated with hemochromatosis, including psoriasis, and possibly hydradenitis suppurativa. So, it might be worth exploring some more, and donating blood in the meantime.


Jedi Master
FOTCM Member
Here’s another good source on the subject:


Sorry I don’t have the exact source at hand, but I remember reading somewhere that e.g. heavy exercise and certain parasites were factors that resulted in the excretion of iron in the hunter-gatherer -times; lack of those factors in the modern time could contribute the accumulation of excess iron.

Anthony Colpo was mentioned in the Chris Kresser podcast, and I remember coming across some of his writings on the issue a while back, fwiw:


The first thing anyone must do before embarking on any iron-reduction regime is to get their iron status tested. Before attempting to lower one’s iron, one should actually determine if it in fact needs lowering.

Yes, brilliant, I know.

Thank you…

No really, thank you….

Seriously, people should forget about phlebotomies, IP-6, lactoferrin/apolactoferrin, drinking ungodly amounts of tannin-rich teas, and dating vampires until they’ve visited their doctor and asked him to check the following (at a minimum):

Serum ferritin
Transferrin saturation

The most crucial one is serum ferritin (as it is the most reliable reflector of overall bodily iron stores) but the other two also supply important information.

Thankfully, you’ve had the wherewithal to already perform this crucial step prior to any iron-lowering attempt. Congratulations, because this automatically shows you are smarter than a good deal of the population. Which isn’t surprising, you being an AnthonyColpo.com reader and all.

Anyway, this is where the fun really starts. And the disclaimers. What follows is what worked for me after much trial and error, anyone who intends to lower their iron in a similar manner should pay close attention to their energy levels, mood, and overall feeling of wellbeing. They should also be under the care of a medical practitioner….if you can find one who has a clue what you’re trying to do.

OK, let’s now begin the story of how I lowered my bodily iron stores without destroying my training in the process…

Despite knowing about the benefits of iron reduction many, many moons ago, it wasn’t until just a few years back that I finally got my serum ferritin down to where I wanted it to be. The problem was that, being an active individual who trains on a daily or near-daily basis, I simply wasn’t able to recover from phlebotomies. Each withdrawal pulls a half-liter of blood from your body, which is a significant loss; the average person has around 5 liters of blood in their body, so we’re talking a 10% loss of total blood volume in a matter of minutes. In sedentary folks, whose oxygen delivery needs are rarely challenged by anything more strenuous than pushing a supermarket trolly or the buttons of a remote control, this isn’t such a big deal.

But for someone whose oxygen delivery needs encompass storming up hills on a bike, doing multiple sets of power cleans, rolling on the mats, doing sprints at the local park, etc, etc, things get a little muddy. Well, they did for me anyway. After withdrawals I’d feel flat and sometimes would even get a slight swelling in my throat.

Not good.

So I went back to the drawing board. In 2008, I sat down for a brainstorming session in my high-tech experimental facility (a.k.a. my kitchen), stared at the 2005 Superman calender on the wall for what seemed like an eternity, then – in a blinding, mind-jolting, reality-transcending flash of light (my little nephew flashed his new Bat Torch in my eyes…) – I came up with what turned out to be a rather sterling plan.

I decided to have blood withdrawals on a monthly basis, until my target serum ferritin was reached. The key change was that, on the weeks I had the withdrawal, I took the entire week off from training and had the phlebotomy mid-week. I trained like an animal with high volume on the other 3 weeks to compensate.

The average reduction in serum ferritin per withdrawal is 30 ng/mL, so I estimated I’d need 6 withdrawals to get down to around 25 ng/mL. This is the recommended target by folks such as the Iron Disorders Institute, and is just above the USA cut-off limit for deficiency (20 ng/mL). Here in Australia, the cut-off point is 30, something I’ll discuss further in just a moment.

As it turns out, I hit 28 after only 5 phlebotomies. I suspect the early arrival was due to my vigorous training regimen.

At this point, I started to feel fatigued during and after bike rides. Going up hills suddenly seemed much harder and my times were slipping backwards. By the time my serum ferritin had increased to 38, I felt fine and was churning out kick-ass times again. So I now give far more credence to the Australian cut-off than the US cut-off. Not because I come from a land Down Under where the women glow and men chunder, but because the US cut-off point is probably way too low for athletic folks – it certainly was in my case.

Unfortunately, the research into iron reduction for athletes is next to non-existent, which is what necessitated my guinea pig approach in the first place. Because my experience constitutes an experiment of 1, I can’t guarantee at exactly what SF level other athletic individuals will experience performance decrements. Hence I strongly recommend the following precautions:

1. Get your SF tested regularly when using phelobotomy, IP-6 or any other iron-reduction strategy. Do not wait until after you estimate you will reach your target SF, because by then you may already be “overbled”.

2. Do NOT overbleed, otherwise you will drop into the deficiency zone. Ask anyone who’s ever been anemic or iron-deficient and they’ll tell you – it sucks. Everything feels like a massive effort, simply getting up out of a chair feels like a 600 lb squat, and as for doing a workout…yeah, right.

3. Closely monitor your energy levels, mood state, etc.

4. Keep a close eye on your performance, via run/ride times, poundages or whatever other measure is used to define performance in your chosen sport.

5. Do not have phlebotomy the day of, before or after a hard workout, trust me, you’ll regret it.

6. Buy yourself a copy of the outstanding Exposing the Hidden Dangers of Iron by Garrison and Weinberg. Ignore the authors’ dismissal of IP6, and realize the recommendation to lower SF to 25 is for sedentary folks…otherwise the book is excellent and contains a wealth of information and is a must read for anyone partaking in iron reduction. I honestly believe it’s one of the best popular-format health books ever written.

If you’re prepared to do all that, then some potentially huge improvements in wellbeing and performance may be just around the corner.

One last thing: most blood donor schemes only allow you to donate blood once every 8-10 weeks. If you have high iron levels and wish to reduce them solely by phlebotomy, this is too infrequent. If you can’t get a doctor to prescribe more frequent phlebotomies, don’t have venipuncture skills or don’t have a family member/girlfriend who is a nurse, then you’re going to have to find a complimentary or alternative strategy.

My first stop would be IP-6, which I used successfully to halve a very high starting SF level several years back. One could use IP-6 exclusively, or in conjunction with blood donation. Why others have not experienced success with it, I can’t say with no further information to work with (dosages, manufacturer, etc). I used a level teaspoon of Source Naturals IP-6 first thing on an empty stomach every morning. I often get people asking me how long they will need to take IP-6 for; refer back to recommendation #1. I am not a clairvoyant, only blood testing can tell you how your iron-lowering efforts are progressing and where your SF is at.

I’ve not used lactoferrin or its variants, and don’t personally know anyone who has, so I cannot comment or vouch for their efficiency, or lack thereof.

Dr Francesco Facchini has used a diet free of red meat and high in phenols, tannins and phytate to dramatically reduce bodily iron stores and greatly improve clinical outcomes in chronic kidney patients. The diet also included dairy and eggs, both of which contain iron-binding elements. I tried this approach in a half-assed manner many years ago (I halved my red meat intake but wasn’t prepared to cut it out entirely, and wouldn’t eat phytate-rich foods like soy and whole-grains in a fit due to their concentration of other unwanted anti-nutrients. This was also well before I’d had my food sensitivities to dairy, eggs et al successfully treated with N.A.E.T). Not surprisingly, it did diddly for me. However, if you want to check out Facchini’s protocol, here’s a link to the full text of his published paper:

A low-iron-available, polyphenol-enriched, carbohydrate-restricted diet to slow progression of diabetic nephropathy

His book The Iron Factor of Aging: Why Do Americans Age Faster? is also a worthy read, but I must again emphasize I personally do not endorse avoidance of red meat, I earnestly believe it is too concentrated a source of valuable nutrients to eschew.

Colpo writes from the point of view of an athlete. I apologise for taking this off topic (please move to an appropriate thread if needed), but reading Colpo's writings, I found it interesting how he moved from low carbing to increasing his carb intake due to his sports performance deteriorating: he noticed that with the amount of glycogen depleting sports he did, his performance suffered as he was unable to replenish the glycogen stores sufficiently with minimal carbs. He seems to make a convincing case (a word of warning, his writing style can get somewhat blunt :-[):



If this is the case, perhaps it is not advisable to do too much strenuous exercise, if one wants to avoid problematic carb sources.


FOTCM Member
This one is available at the link below. I didn't read it in detail, but the stats were interesting

Ann Hepatol. 2012 May-Jun;11(3):294-300.
Treatment of hyperferritinemia.
Beaton MD, Adams PC.



Elevated serum ferritin, or hyperferritinemia, is a common finding on routine bloodwork and often prompts referral for further evaluation. In the following review, we outline the various causes of hyperferritinemia and point out that, in the majority of cases, this does not represent true iron overload. Despite much research interest in this area, the precise mechanism of hyperferritinemia and its impact on disease severity in various clinical conditions continues to be debated. While some research suggests that iron reduction in cases of hyperferritinemia is of benefit, the decision to treat such patients should be individualized, and may be influenced by the presence of other features of iron overload.


Serum ferritin is the most frequently requested
measure of body iron status and one of the most fre-
quently requested laboratory tests in both primary
care and referral settings.

Ferritin is the cellular
storage protein for iron and is able to store up to
4,500 atoms of iron with much of this iron accessi-
ble for metabolic needs. The normal adult total body
iron content is approximately 3-4 g. On average, 2.5
g is contained within hemoglobin in circulating red
blood cells and developing erythroblasts, 400 mg in
iron containing proteins, 3-7 mg in the form of
transferrin-bound iron and the remainder stored as
ferritin or hemosiderin.
The human body has no means of excreting ex-
cess iron. Only a very small amount, average 1 mg,
leaves the body each day via loss in sweat, shed skin
cells and some gastrointestinal loss. The vast majo-
rity (20-25 mg) is efficiently recycled from the
breakdown of senescent red blood cells within the
reticuloendothelial system. The average Western
male consumes 1-2 mg of heme iron and 10-15 mg of
non-heme iron each day. Roughly 30% of heme iron
is absorbed and 10% of non-heme iron, totaling 1-2
mg/day maintain iron balance.
Ferritin is a reliable surrogate marker of body
iron stores with low values providing absolute evi-
dence of reduced reticuloendothelial iron stores.

Elevated ferritin levels however, are far less specific
for systemic iron overload. Ferritin is an acute pha-
se reactant, defined as a protein whose serum con-
centration increases or decreases by at least 25
percent during inflammatory states.

The magnitude of the problem of hyperferritine-
mia was evidenced by the results of the HEIRS stu-
This population based screening study sought
to determine the incidence of hereditary hemochro-
matosis (HH) in a large multi-ethnic, multi-racial
primary care setting within North America. Of the
101,168 participants screened for iron overload and
HFE mutations, 5.9% of Caucasian subjects and
19% of Asian subjects were found to have hyperfe-
. Whereas 0.44%, (approximately 1 in 200)
of Caucasians were found to be homozygous for the
C282Y mutation only 0.00004% (1 in 25,000) Asians
were homozygous
. This important study demonstra-
ted that hyperferritinemia is very common and that
in the majority of individuals it is due to conditions
other than HH.

[skipped a lot]


In recent years there has been a great deal of inter-
est regarding the relationship between markers of in-
flammation and health outcomes. It is now well
recognized that activation of inflammatory mediators
plays a significant role in the pathogenesis of many
disease processes that had previously been thought
to be unrelated to inflammation. These include type
2 diabetes (DM2), obesity and other conditions com-
prising the metabolic syndrome (MS). As well there
is increasing evidence supporting the role of inflam-
mation in vascular disease.

As stated previously, hyperferritinemia is consi-
dered an acute phase reactant and as such is eleva-
ted in states of systemic inflammation. A number of
studies have evaluated the association of hyperferri-
tinemia with disease risk and outcome
. Two recent
large, population based studies found that high
serum ferritin levels are associated with an increa-
sed risk of MS and DM2.

Importantly, this in-
creased risk was present among non-obese adults, a
group whom would not normally be considered at
significant risk for these conditions.

There is also some evidence to support a link bet-
ween excess iron and malignancy, specifically hepa-
tocellular carcinoma (HCC). The increased risk of
HCC is well recognized in patients with HH.

Even in the absence of HH, individuals with excess liver
iron have a higher risk of HCC.

The relationship between hyperferritinemia and
vascular disease
has also been supported by recent
studies. A cohort of otherwise healthy young men
was evaluated to determine whether elevated serum
ferritin was associated with decreased levels of car-
diovascular fitness (CVF).

Interestingly, serum fe-
rritin levels > 150 μg/L, which is lower than what is
normally considered to be elevated, were associated
with poorer CVF
. Additional studies have examined
the relationship between ferritin levels and periphe-
ral artery disease (PAD), concluding that hyperferri-
tinemia is associated with the presence of PAD
, and
in one study was associated with an increased risk
of mortality from PAD.

Likely the area of greatest interest regarding a
potential relationship between hyperferritinemia and
disease is in the setting of nonalcoholic fatty liver
(NAFLD). Support for this comes from the
results of large, population based studies. In the
Nurse’s Health Study of over 30,000 healthy wo-
men, it was concluded that and elevated serum ferri-
tin was associated with an increased risk of type 2

Similar results were noted in cohort of
over 6,000 patients participating in the Third Natio-
nal Health and Nutrition Examination Survey
(NHANES III) where the metabolic syndrome was
significantly more common in those with and eleva-
ted serum ferritin.

A recent study demonstrated
that elevated serum ferritin was associated with
worsened histologic activity of NAFLD and was an
independent predictor of advanced hepatic fibrosis.

The term “dysmetabolic iron overload syndrome”
has even been coined to describe this subgroup of
NAFLD patients.

Studies have been published regarding the poten-
tial pathophysiologic role of iron in NAFLD.

One widely supported view is that iron accumulation
leads to increased oxidative stress and lipid peroxi-
dation, both of which are central to the pathophy-
siology of NAFLD. Iron is capable of catalysing the
formation of reactive oxygen (ROS) species and a
number of studies have demonstrated that hepatic
iron loading leads to oxidative damage.



FOTCM Member
Ailén said:
I've also read that there are several skin conditions associated with hemochromatosis, including psoriasis, and possibly hydradenitis suppurativa. So, it might be worth exploring some more, and donating blood in the meantime.

That is an interesting line of inquiry. It seems iron chelators are used to rejuvenate the skin because of iron's role on damaging/oxidizing the skin:

J Cosmet Dermatol. 2006 Sep;5(3):210-7.
Iron chelators may help prevent photoaging.
Kitazawa M, Iwasaki K, Sakamoto K.

AminoScience Laboratories, Ajinomoto Co., Inc., Kawasaki, Japan.


For years, cosmetic ingredients for anti-aging treatments have attracted consumers. Skin aging is accelerated by reactive oxygen species (ROS), generated by exposure to solar ultraviolet radiation (UVR), in a process known as photoaging. Because cutaneous iron catalyses ROS generation, it is thought to play a key role in photoaging. Iron is essential to almost all forms of life. However, excess iron is potentially toxic as its catalytic activity induces the generation of ROS. Iron-catalysed ROS generation is involved in numerous pathological conditions, including cutaneous damage. When skin is directly exposed to UVR, cutaneous intracellular catalytic iron levels increase because of the release of iron from iron-binding proteins such as ferritin. Consequently, the subsequent ROS generation may overwhelm cutaneous defense systems such as the cellular iron sequestration and ROS scavenging capacity. The harmful role of excess cutaneous iron implies that there may be a potential for topical iron chelator treatments. We now consider cutaneous photodamage skin photoaging as the result of iron-catalysed ROS generation and discuss preventative strategies based on iron chelators.

This seems to connect ferritin and sun exposure skin damage seen in so many autoimmune diseases, being lupus and its related diseases the classic one!


The Living Force
Mrs. Peel said:
I'm trying to read all this info but it's really making my eyes hurt, so is eating something that binds to iron good or bad? If it means you won't absorb it and you have high iron, that's good? Or conversely, if you are low in iron, and you eat foods that bind to it, you don't absorb it and can become anemic, and that's bad, right?

Yes, I think that's how it works and you're understanding it correctly.


FOTCM Member
You can get a relatively inexpensive genetic test here:



FOTCM Member
Amazing how expensive some of those books are! It's like they really don't want the average person to have access to that information! Even if it is not planned and deliberate, that is the effective result.
Top Bottom