by Sea at 05-14-2016, 09:52 AM
Email response from Ray Peat regarding DMSO Feb 24 2016:

I got interested in it in 1965, after reading about Stanley Jacob’s ideas, and experimented with it occasionally over the next several years. I was interested in its effects on cell water, stabilizing it in a way that reduces some kinds of inflammation. It seems to accelerate some enzyme reactions.  I later started to think about its own chemical properties, rather than thinking of it as just a solvent. It isn’t stable in the presence of water, and the odor seems to indicate the degree of its decomposition. It occasionally helps slightly with joint pain, but it can cause intense skin reactions, rashes; I think some of its effects depend on the breakdown products. People often forget that it has an intrinsic oxidative effect when they are thinking of it as just a solvent, to transport drugs. I saw a product sold as eye drops, consisting of vitamin C and glutathione in DMSO. Each of those reductants, in the presence of DMSO, immediately breaks down into other substances, and the composition changes continually over a long period. There has been very little investigation of the actual composition of solutions of DMSO with other substances. At least some of the mixtures will produce sulfite and metabisulfite, which are very allergenic for some people. Small amounts are probably harmless; even large amounts seem harmless for some people. Its ability to release histamine and nitric oxide and to inhibit cholinesterase (articles below) suggest that its use shouldn’t be prolonged.

Arch Dermatol. 1988 Feb;124(2):182-3.
Systemic contact dermatitis medicamentosa occurring after intravesical dimethyl
sulfoxide treatment for interstitial cystitis.
Nishimura M, Takano Y, Toshitani S.

Eye (Lond). 2001 Jun;15(Pt 3):332-3.
Lens deposits associated with RIMSO-50 (dimethylsulphoxide).
Rowley S, Baer R.

Cornell Vet. 1986 Jan;76(1):61-90.
Dimethyl sulfoxide (DMSO): a review.
Brayton CF.
Dimethyl sulfoxide (DMSO) is a very simple compound that has stimulated much
controversy in the scientific and popular literature. Fig. 1 It is an aprotic
solvent. Therapeutic and toxic agents that are not soluble in water are often
soluble in DMSO. DMSO has a very strong affinity for water; on exposure to air,
pure DMSO is rapidly diluted. DMSO's physiologic and pharmacologic properties and
effects are incompletely understood. Properties that are considered to be
particularly important to its therapeutic and toxic effects include: its own
rapid penetration and enhanced penetration of other substances across biologic
membranes; free radical scavenging; effects on coagulation; anticholinesterase
activity; and DMSO-induced histamine release by mast cells. DMSO's systemic
toxicity is considered to be low. Combinations of DMSO with other toxic agents
probably constitute its greatest toxic potential. The scientific literature is
reviewed with particular attention to mechanisms underlying DMSO's reported
therapeutic and toxic effects. Currently approved, veterinary applications of
DMSO are limited. DMSO's potential value in specific, approved and unapproved
veterinary applications is discussed.

Ukr Biokhim Zh (1999). 2001 Jul-Aug;73(4):114-9.
[Potentiation of the cataractogenic effect of light by dimethylsulfoxide and
[Article in Russian]
Metelitsyna IP(1).
(1)Filatov Institute of Eye Diseases and Tissue Therapy, Academy of Medical
Sciences of Ukraine, Odessa.
On the basis of the data about possible potentiation of polychromatic light
cataractogenic effect by adrenaline and dimethylsulfoxide preparations, obtained
by us earlier (increasing of animals number with changes of lenses and metabolic
disturbances, of the first clinical signs of cataract in more earlier terms, more
rapid development occurred in lenses opacities, more intensive changes of lenses
substance), we have studied some biochemical parameters (peroxide resistance of
erythrocyte, the level of free amine nitrogen, activity of Na,K-ATP-ase,
gamma-glutamiltranspeptidase, ceruloplasmin) in blood, liver and tissues of
rabbits eyes, during modelling of the light cataract on the background of
supplementary application of adrenalin and dimethylsulfoxide. It was shown that
one of the possible mechanisms of cocataractogenic action of the studied
substances is the revealed fact of increasing the metabolic systems disturbances,
caused by long-term irradiation of the animals.

AJNR Am J Neuroradiol. 1999 Mar;20(3):401-10.
A reexamination of the angiotoxicity of superselective injection of DMSO in the
swine rete embolization model.
Chaloupka JC(1), Huddle DC, Alderman J, Fink S, Hammond R, Vinters HV.
(1)Department of Diagnostic Radiology, Yale University School of Medicine, USA.
BACKGROUND AND PURPOSE: There are a variety of embolization applications for
non-adhesive, liquid agents. We reevaluated the potential microvascular
angiotoxicity of superselective infusions of dimethyl sulfoxide (DMSO) using very
long infusion rates in a previously described animal model.
METHODS: Twenty-six swine underwent percutaneous femoral puncture for
superselective catheterization of the artery of the rete while being continuously
monitored for ECG and intraarterial pressure. Two volumes (0.5 or 0.8 mL) and
three durations (30, 60, and 90 seconds) of superselective infusion of DMSO were
used to evaluate the effect of a single-dose rate within an ipsilateral rete.
Contralateral control infusions of normal saline were also administered. Acute
hemodynamic and angiographic outcomes were assessed. After recovery, follow-up
angiography and sacrifice were performed at either 10 or 28 days. Brains and
retia were harvested for gross and microscopic histopathologic evaluation.
RESULTS: No significant hemodynamic alterations occurred acutely. Twenty-three of
the 24 infused retia showed variable acute vasospasm that typically was mild to
moderate in severity and transient (10 to 20 minutes). Follow-up angiography at
sacrifice always showed normal retial arterial anatomy. No adverse clinical
sequelae were noted. Gross inspection of brains showed no evidence of infarction
or subarachnoid hemorrhage. Microscopic histopathologic examination of retia
showed mostly nonspecific changes in both exposed and control samples. Possible
causal histotoxicity was seen in four retia (three of four exposed to higher dose
rates), in which involvement was limited to one to three retial arteries.
CONCLUSION: Lower total dose and dose rates of superselective infusion of DMSO
into the retial microarterial network resulted in substantially less
angiotoxicity than that found in a previous study, as defined by clinical,
angiographic, gross, and histopathologic criteria.

Anticancer Res. 1998 Nov-Dec;18(6B):4705-8.
Clinical toxicity of cryopreserved circulating progenitor cells infusion.
Zambelli A(1), Poggi G, Da Prada G, Pedrazzoli P, Cuomo A, Miotti D, Perotti C,
Preti P, Robustelli della Cuna G.
(1)Divisione di Oncologia Medica, IRCCS Fondazione S. Maugeri, Centro Medico di
Pavia, Italy.
 BACKGROUND: We evaluated the infusion-related toxicity of cryopreserved
autologous circulating progenitor cells transplanted in 22 patients receiving
high dose chemotherapy and stem cells transplantation for malignancy.
MATERIALS AND METHODS: Progenitor cells were collected following mobilization
with chemotherapy plus filgrastim and stored in liquid nitrogen in the presence
of 10% dimethylsulfoxide (DMSO). Before infusion of the graft, patients were
medicated with mannitol, hydrocortisone and clorphenamine. The amount of DMSO
infused as well as the number of dead and damaged cells were evaluated as
possible cause of toxicity.
RESULTS: Eleven patients (50%) experienced symptoms related to graft infusion,
nausea and vomiting being the most common adverse events. Hypotension was
documented in 3 patients (one of them developing transient bradycardia resolved
with atropin administration) and one had hypertension with tachycardia. Other
observed side effects were: chest tightness (2 pts), fever and chills (3 pts),
associated with abdominal cramps (2 pts). 7 out of 8 (88%) patients infused with
greater than 30 mL volume of DMSO experienced side-effects, the grade of toxicity
being significantly less in those receiving lower amount (< 30 mL) of DMSO. Two
out of 4 pts who received the highest number of dead cells (> 10 x 10(9))
developed toxicity.
CONCLUSIONS: In our experience the infusion of cryopreserved peripheral blood
progenitors caused minor to moderate toxicity in most cases and, when present,
side effects were observed only during infusion. The amount of DMSO present in
the graft is related to the grade of toxicity.

Cytotherapy. 1999;1(6):439-46.
Post-thaw removal of DMSO does not completely abrogate infusional toxicity or the
need for pre-infusion histamine blockade.
Rowley SD(1), Feng Z, Yadock D, Holmberg L, Macleod B, Heimfeld S.
(1)Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle,
Washington, USA.
BACKGROUND: The infusion of PBSC or BM cells cryopreserved with DMSO is
associated with frequent, but generally minor, toxicity. The incidence and
severity of infusion-related toxicity is proportional to the amount of DMSO
infused. In an attempt to reduce the incidence of symptoms reported by patients
receiving cryopreserved PBSC and to avoid the necessity of diphenhydramine
premedication, we studied the infusion of PBSC components from which the DMSO was
depleted after thawing.
METHODS: This was a Phase I/II study of post-thaw removal of DMSO. Patients
undergoing autologous PBSC transplantation with components cryopreserved using
10% DMSO were eligible. The PBSC components were thawed, diluted with 10%
dextran-40 and 5% HSA, centrifuged to remove the DMSO, resuspended in dextran and
HSA, and infused without prior medication of the patient. Visual analog scale
questionnaires were used for measurement of infusion-related symptoms.
RESULTS: Five patients were enrolled on this study and received washed PBSC
components. One patient experienced severe infusion-related toxicity and the
study was stopped for safety reasons. Events experienced by these patients
included flushing (two patients), emesis (three patients), and post-infusion
rigors (two patients). Two patients reported an increase in nausea after the
infusion. All patients achieved granulocyte engraftment (an ANC > 0.5 x 10(9)/L)
at a median of 14 days and platelet engraftment (platelet count without
transfusion > 20 x 10(9)/L) at a median of 11 days. No patient required infusion
of additional cells because of engraftment failure.
DISCUSSION: In theory, the post-thaw reduction of DMSO should reduce the risk of
infusion-related toxicity that is commonly attributed to DMSO. Although not
demonstrated by the data developed from this study, effective reduction in DMSO
could also eliminate the need for pre-infusion histamine blockade. However, the
technique used in this study was not adequate and a more rigorous depletion
technique must be developed to completely abrogate clinical infusion-related

Cell Biol Int. 2005 Jul;29(7):529-36.
NF-kappaB and NOS may play a role in human RPMI-8402 cell apoptosis.
Trubiani O(1), Salvolini E, Vignini A, D'Arcangelo C, Di Primio R, Mazzanti L.
(1)Dipartimento di Scienze Odontostomatologiche, Università di Chieti-Pescara,
Via Dei Vestini, 35, 66100 Chieti, Italy.
Apoptosis is a fundamental process that is required for the normal development
and functioning of the immune system. It can be induced in different ways
depending on cell type and acquired signal. Since the NF-kappaB transcription
factor complex is believed to be involved in nitric oxide-induced apoptosis, the
aim of this study was to investigate NF-kappaB and nitric oxide synthase (NOS)
activity during dimethyl sulphoxide (DMSO)-dependent cell death of RPMI-8402
human pre-T cells. Our results show that NF-kappaB activation is associated with
a significant up-regulation of NOS activity and induction of apoptosis.
Furthermore, the inhibition and reversal of these effects by parthenolide
treatment or DMSO removal indicate that these molecules are directly involved in
the progression of cell death.

Int J Immunopathol Pharmacol. 2003 Sep-Dec;16(3):253-9.
DMSO modifies structural and functional properties of RPMI-8402 cells by
promoting programmed cell death.
Trubiani O(1), Salvolini E, Staffolani R, Di Primio R, Mazzanti L.
(1)Dipartimento di Scienze Odontostomatologiche, University of Chieti, Italy.
Apoptosis in lymphoid cells can be induced in different ways depending on cell
type and acquired signal. Biochemical modifications occur at an early phase of
cell death while at late times the typical morphological features of apoptosis
can be visualized. The aim of this study is to verify by multiparametric analyses
the plasma membrane fluidity, the intracellular Ca2+ concentration and the nitric
oxide synthase (NOS) activity during cell death progression induced by DMSO
treatment. The RPMI-8402 human pre-T lymphoblastoid cell line was induced to cell
death by DMSO. Analyses rescued at early times of treatment prove a substantial
modification of plasma membrane fluidity associated with an increase of
intracellular Ca2+. Moreover, these modifications are associated with an up
regulation of NOS activity. Our results are consistent with the hypothesis that
programmed cell death can be induced by up regulation of the intracellular Ca2+
associated with an increase of cell membrane fluidity. The apoptotic mechanisms
seem to involve not only membrane damage and increased intracellular calcium
levels but also production of nitric oxide.

Vet Hum Toxicol. 1998 Apr;40(2):87-9.
Sulfhemoglobinemia after dermal application of DMSO.
Burgess JL(1), Hamner AP, Robertson WO.
Author information:
(1)Washington Poison Center, Seattle 98125-8012, USA.
   A 43-y-old Caucasian female applied 4 ounces of dimethyl sulfoxide (DMSO) to her
lower abdomen for treatment of interstitial cystitis. Within 24 h she developed
fatigue, cyanosis and dyspnea with mild exertion. She sought medical attention 10
d later, at which time initial laboratory tests revealed a methemoglobin level of
47%. Two doses of 1 mg methylene blue/kg i.v. were given without significant
improvement in either her cyanosis or methemoglobin level. Repeat analysis the
day following admission using an outside lab demonstrated a sulfhemoglobin level
of 6.2% and a methemoglobin level of < 0.1%. No prior reports have associated
sulfhemoglobin formation with DMSO application. Carbon monoxide-oximetry may
falsely identify sulfhemoglobin as methemoglobin; sulfhemoglobinemia should be
considered in cases of methemoglobinemia refractory to methylene blue therapy.

Nephron. 1996;72(2):356-7.
Multiple organ failure associated with dimethylsulfoxide and hydroxyethyl starch
in autologous blood stem cell transplantation.
Nishihara G, Sakemi T, Ikeda Y, Baba N, Shimamoto Y.

Contact Dermatitis. 1998 Feb;38(2):90-5.
Susceptibility to skin stinging, non-immunologic contact urticaria and acute skin
irritation; is there a relationship?
Coverly J(1), Peters L, Whittle E, Basketter DA.
(1)Unilever Environmental Safety Laboratory, Sharnbrook, Bedford, UK.
  Adverse skin reactions cover many types of response: toxic, irritant, allergic,
urticarial, sensory, etc. The relationships between an individual's tendency to
develop different types of skin response are not well-described. We examined
whether those who perceive stinging might be more likely to experience
urticarial, sensory and irritation reactions in skin. A panel of 86 volunteers
was tested with 10% lactic acid in the nasolabial fold to assess their ability to
perceive stinging. At the same time, their capacity to develop non-immunologic
contact urticaria was evaluated using chemicals of different structural type and
urticant ability: methyl nicotinate, benzoic acid, cinnamic acid, cinnamaldehyde
and dimethyl sulfoxide (DMSO). DMSO was also used to assess sensory effects and
skin irritation. 44 were classes as "stingers" and 42 as "non-stingers". The
pattern of urticant reactivity in the stingers and non-stingers was essentially
the same, with neat DMSO generating the strongest reactions in both groups.
Sensory reactions to DMSO (stinging, itching, tingling or burning) were similar
in stingers and non-stingers; although the former may have reacted more quickly,
a smaller proportion reacted (64% versus 76%). The skin irritation response to
DMSO was also identical in stingers and non-stingers and the intensity of the
urticant response in an individual did not correlate with the intensity of their
subsequent irritant reaction. In conclusion, this study demonstrated that an
individual's ability to perceive skin stinging does not give a general indication
of their susceptibility to other types of non-immunologic skin response. Indeed,
there appeared to be little evidence of correlations between any of the skin
effects studied.

Urology. 1981 Jul;18(1):21-6.
Prospective study of intravesical dimethyl sulfoxide in treatment of suspected
early interstitial cystitis.
Fowler JE Jr.
The efficacy of intravesical instillations of dimethyl sulfoxide (DMSO) in the
treatment of suspected early interstitial cystitis was investigated in a
prospective study. Among 20 patients treated, complete symptomatic remissions
were achieved in 3, partial symptomatic remissions were achieved in 16, and 1 had
no symptomatic improvement. However, functional bladder capacities following
treatment were increased by more than 25 per cent in only 4 cases. Among 16
patients who experienced symptomatic remissions and who have been followed for
greater than or equal to four months, 14 had sustained remissions (mean follow-up
eleven months) and 2 had unsustained remissions. Clinically apparent toxicity was
minimal but transient elevation of the serum lactic acid dehydrogenase was
occasionally observed during treatment. DMSO appears to be useful in the
management of carefully selected patients with suspected early interstitial

Lancet. 1981 Jan 31;1(8214):276-7.
Dimethylsulphoxide toxicity.
Greenfield C.

Med Sci Sports Exerc. 1981;13(4):215-9.
The use of DMSO in tennis elbow and rotator cuff tendonitis: a double-blind
Percy EC, Carson JD.
Over a 1-yr period, 102 patients with a clinical diagnosis of either medial or
lateral epicondylitis (tennis elbow) or rotator cuff tendonitis were treated with
topical applications of dimethyl sulfoxide (DMSO). A double-blind controlled
study was carried out on these patients in the private practice of an orthopaedic
surgeon to determine the efficacy of this material in the treatment of these two
common clinical conditions. Beneficial effects were assessed with respect to
improvement in pain, tenderness or swelling, and increase in the range of motion.
Forty patients were treated for each of the two ailments; patients treated with
the 70% DMSO aqueous solution did not receive any more beneficial effect from the
drug than patients who received 5% DMSO aqueous placebo solution.

Lancet. 1980 Nov 8;2(8202):1004-6.
Dimethylsulphoxide-induced toxicity.
Yellowlees P, Greenfield C, McIntyre N.
Two elderly people were given intravenous infusion of dimethylsulphoxide (DMSO)
as treatment for arthritis. One became seriously ill, the other remained well.
Both had similar changes in aspartate transaminase, hydroxybutyrate
dehydrogenase, and creatine kinase and evidence of haemolysis. This is the first
report of serum enzyme changes and anaemia after intravenous DMSO in man.

Med Monatsschr. 1974 Aug;28(8):325-6.
[Dimethyl sulfoxide is not dead].
[Article in German]
Simon KH.

Med Klin. 1974 Oct 18;69(42):1683-8.
[Iatrogenic cataracts].
[Article in German]
Koch HR, Hockwin O.

Am J Optom Arch Am Acad Optom. 1972 Apr;49(4):308-19.
Cataracts induced in guinea pigs by acetone, cyclohexanone, and dimethyl
Rengstorff RH, Petrali JP, Sim VM.

CRC Crit Rev Toxicol. 1971 Sep;1(1):93-118.
The cataractogenic activity of chemical agents.
Gehring PJ.

Arch Geschwulstforsch. 1971;37(1):1-3.
[Question of carcinogenic action of dimethyl sulfoxide (DMSO)].
[Article in German]
Lohs K, Damerau W, Schramm T.

Ophthalmologica. 1969;158 Suppl:488-93.
Changes in rabbit lenses following DMSO therapy.
Wood DC, Wirth NV.

Int Ophthalmol Clin. 1970 Fall;10(3):553-619.
Some iatrogenic ocular diseases from systemically administered drugs.
Bernstein HN.

J Pharmacol Exp Ther. 1969 Dec;170(2):364-70.
The ocular effects of repeated dermal applications of dimethyl sulfoxide to dogs
and monkeys.
Smith ER, Mason MM, Epstein E.

Northwest Med. 1969 Jan;68(1):39-41.
Eye effects of DMSO. Report of negative results.
Hull FW, Wood DC, Brobyn RD.

Schweiz Med Wochenschr. 1968 Nov 16;98(46):1829-37.
[About some effects of dimethyl sulfoxide (DMSO) in percutaneous use].
[Article in German]
Kappert A.

Exp Pathol (Jena). 1975;10(5-6):364-5.
Tumor-inducing effect of trinitroso-trimethylene-triamine (TTT) when orally
applied in dimethylsulphoxide (DMSO) for solvent.
Urban H, Amlacher E, Danz M.
By oral application of TTT, disolved in concentrated DMSO, it was possible by
means of a long-term experiment to produce tumors in female rats (Wistar strain).
Contrary to all previous findings the tumor-inducing effect of this substance has
been proved in this way for the first time.

Ann Hematol. 2015 Mar;94(3):511-3.
DMSO induced myocardial infarction during allogeneic cryopreserved bone marrow
Khawandanah M(1), Hopps S, Nabeel S, Ahmad B, Weiss S, Holter Charkrabarty J,
Yuen C, Selby G.
(1)Hematology-Oncology Section, Department of Medicine, The University of
Oklahoma Health Sciences Center, Oklahoma City, OK, USA,

Ann Hematol. 2013 Nov;92(11):1571-2.
Severe vasospastic angina with hemodynamic compromise related to the infusion of
dimethyl sulfoxide (DMSO)-cryopreserved autologous peripheral blood stem cells.
Bambace NM(1), Lachance S.
(1)Blood and Marrow Transplant Program, Division of Hematology and Medical
Oncology, Hôpital Maisonneuve-Rosemont, Université de Montréal, 5415 Boul. de
L'Assomption, Montreal, Quebec, H1T 2M4, Canada,

Ann Pharm Fr. 1970 Apr;28(4):263-70.
[Damage of limb buds of chicken embryos by dimethyl sulfoxide].
[Article in French]
Cros S, Voisin MC, Tollon Y, Oreglia J.

Int Ophthalmol Clin. 1971;11(2):63-97.
Effects of drugs on the lens.
Paterson CA.
PIP: The effects of drugs that cause changes in the lens, principally cataractous
changes, are discussed. The cataractogenic compounds reported on include 1) drugs
used in ophthalmic practice (miotics and topical steroids), 2) compounds used in
systemic therapy of a wide range of disorders (corticosteroids
andphenothiazines), and 3) compounds that are known to be cataractogenic in
animals but not in man (Myleran). Of special interest to family planners is a
section on the effects of oral contraceptives on lens changes. Whether long-term
use of oral contraceptives would produce ocular complications was queried by
Cogan. The influence of these drugs on ocular tissues was subsequently studied,
but no significant lens changes were described. Other ocular abnormalities were,
however, detected. In rabbit studies, it was shown that mestranol in
norethynodrel caused anterior lens changes. Cataracts and other lesions were
produced in rats fed a synthetic progestin-estrogen. In vitro changes in lens
permeability caused by progestins and progestins and estrogens were demonstrated
by Lambert. A dose-dependent increase in rubidium-86 efflux (a measure of lens
cell permeability) was demonstrated for several progestins and estrogens. An
alteration in cation and water content and lens clarity was also observed. Such
physiological changes are similar to those induced by progestins and estrogens in
erythrocytes, mitochondria, and lysosomes. It is noted that although the
concentrations of drugs used in animals and in vitro studies are high, there is a
need for well-controlled, long-term opthalmological studies on women who have
chosen oral contraceptives.

Fortschr Ophthalmol. 1988;85(4):396-9.
[Significance of experimental cataracts for the development of senile cataracts
exemplified by naphthalene and dimethyl sulfoxide-induced lens opacities].
[Article in German]
Rossa V, Kluxen G.

Ann N Y Acad Sci. 1975 Jan 27;243:98-103.
Toxicity of dimethyl sulfoxide, alone and in combination.
Rubin LF.

Med Klin. 1974 Oct 18;69(42):1683-8.
[Iatrogenic cataracts].
[Article in German]
Koch HR, Hockwin O.

Invest Ophthalmol. 1974 Oct;13(10):713-24.
Mechanisms initiating cataract formation. Proctor Lecture.
Kinoshita JH.

Exp Eye Res. 1972 Sep;14(2):91-8.
Some changes in the lens of the dimethylsulphoxide-fed rabbit.
Van Heyningen R, Harding JJ.

CRC Crit Rev Toxicol. 1971 Sep;1(1):93-118.
The cataractogenic activity of chemical agents.
Gehring PJ.

Int Ophthalmol Clin. 1970 Fall;10(3):553-619.
Some iatrogenic ocular diseases from systemically administered drugs.
Bernstein HN.

Radiology. 1969 Jan;92(1):156-8.
Anomalous effects of dimethyl sulfoxide on the response of the mouse lens and
cornea to x-irradiation: "protection" of lens and "sensitization" of cornea.
Hagemann RF, Evans TC, Riley EF.

Ann N Y Acad Sci. 1967 Mar 15;141(1):392-401.
Dimethyl sulfoxide in ophthalmology, with especial reference to possible toxic
Gordon DM.

Br Vet J. 1971 Jul;127(7):301-3.
Drug-induced lenticular lesions in the dog.
Heywood R.
by ChasingGoodandEvil at 05-13-2016, 10:25 PM
Besides fructose and gelatin, any tricks for raising low cholesterol? I was thinking vitamin k2, as i only consume 1mg/day. It's for my girlfriend, she doesn't like carrot salad, already consumes a fair amount of aspirin. Currently on 1.25 grains armour. Cholesterol was148. Appreciate any suggestions.
by Sea at 05-10-2016, 06:14 AM
I am still adjusting the recipe, but I wanted to post to give an idea for people new to eating sugar, how it can be done.

1 pound 90% lean ground beef
1 cup refined white sugar
1 cup tomato sauce
1 cup strong coffee(2x+ coffee grounds/cup)
2 tablespoons salt

Heat a large pan and add all the ingredients, then chop up the beef into bite sized pieces with a spatula. If your pan is smaller you might want to add the beef last after you have stirred the sugar into the other ingredients.

Nutrition facts:
Carbohydrates 215g/860 calories
Protein 90g/360 calories
Fat: 48g/432 calories
by Arborescence at 05-08-2016, 01:11 AM
Hi guys,

My gut is really messed up since taking a lot of antibiotics for Lyme 4 years ago. It destroyed my gut and vascular system (I know when my nitric oxide increases, because my varicocele increase and dark circle under the eyes become very dark) :
I also have deformities in the joints (probably Ehler's Dandros or Marfan syndrome).
I think my lymph nodes are kind of hard (fibrosis ?) and inflammed.

I can't tolerate any starches or insoluble fibers like in apples or bananas (even milk gives me a runny nose), and I am a student so I don't have a lot of money. The only fibers that seemed fine were bamboo shoots but it's very expensive and hard to source here, even the raw carrot or mushrooms are not good for me.
All I can do is to eat fruits like peaches (I'm buying a cooked peaches compote with 15% sugar) and a bit of melons/mangoes from times to times and a lot of orange juice. I don't get much manganese or molybdenum in my diet.
Things like BCAA and activated charcoal helped with gut inflammation/endotoxins (I'm almost taking it everyday because like would be a disaster without it) but I still can't eat any starches (even very well cooked rice or potatoes), it makes me feel depressed and fatigued, same for other fibers.

I've tried different amounts of proteins but 100g/day seems fine for me (even better since taking a bit of BCAA, tyrosine and lysine), if I take less I can get some kind of spasms in the liver.
My main issue is that I crave sugar everytime and can't go without food for more than 1 hour or else I will start to become tired (I tink I'm eating up to 300 or 400g of sucrose/day) and have an increase in attention disorder and anhedonia (not good for school).
I've put on a lot of weight as I think I'm eating too much calories (I'm eating 3000 or 4000 calories/day, sometimes  bit less, I'm 6'5 and 25 years old) and I think the new fat tissues are making a lot of aromatase.
4 month ago I ate a pufa meal and the following day I've started to get gynecomastia in the left breast (inflammed cyst and more fat in this breast than in the other). I've tried everything on it (methylene blue, haidut Estroban, vitamin E, vitamin A, aspirin, liquid glycine, etc). Sometimes things help to lower inflammation but it's only momentary.

I had to stop Tyromax from idealabs (2 days ago) because I could not tolerate the DMSO (I think it made me stressed), I will start to take my temps again to see how things go without Tyromax.

Too much fluids make me feel cold and stressed (and give me hypertension) so I can't take too much milk and orange juice for calories.

Things like methylene blue and Co-enzyme Q10 help me, everytime I get stressed I can see the dark circles worsening.
Would you have any advices for me please?

Thanks Wink.
by ChasingGoodandEvil at 05-07-2016, 07:11 PM
Havesome contributions to make from ray pat email. Seems kind o lersonal to post but i pomksed that if i wass given his email address, i would share the correspondence, and ofcourse now i cant nor want to post on raypeatforum. I think ray doesnt get very personal with his emails, just wants the info out there, so i'd be happy to share.
by ChasingGoodandEvil at 05-06-2016, 11:57 PM
I hate tv and media, i don't understand how anyone can be so retarded to trust anything these bitches say. You can practically see their labias! I don't trust any journalist, especially who spread their legs to announce the news.
by flipflop at 05-02-2016, 09:19 PM
Hi There,

I seem to be running on adrenaline pretty constantly.. 
Recently I tried pushing up my calories because I think i've pretty much under eaten most of my life due to severe stress.. About a year ago I had an intense period of stress that messed me up so bad that I now have had sleep issues for a year.. I've been taking cypro for the past 9 months at 4-8 mg a day.. I've had chronic fatigue issues for 20 years and i think this may have been due to undereating.. 
Since pushing my calories up I've increased my fat consumption and my adrenaline seems to have gotten worse..
I jut started taking NDT today to see if it will help bring my adrenaline down. Cortisol doesn't seem to rise as much as adrenaline but that might be due to having had high cortisol all my life?

I'm currently eating around 450 gms of carbs a day from roots, white rice, fruit and sugar.
I also seem to have a resting tremor which I only notice when I lie down , possibly form cortisol.. My sleep is a nightmare .. I can;t fall asleep without ambien..

I'm getting a little sick of this.. I have not had too many blood tests.. but the ones I did have showed low ferritin, high cholesterol, low copper, low ceruloplasm, TSH was around 2.3 ..Platelet count was low. I think many of these numbers are a reflection of someone starving but the otehr thing i seem to have now is no appetite so I have to literally force myself to eat . It's all very challenging.. If anyone has any suggestions I'm all ears 

my daily food intake looks around 3000 cals if I can get it in me. Made up of mostly peaty foods.. I did try eating some wheat in order to try and get more variety a few weeks ago but ended up feeling really depressed so I cut it back out ..

Thank you
by Arborescence at 04-27-2016, 02:16 AM
The original post was requested to be deleted by the author.
by Sea at 04-27-2016, 01:40 AM
Candy is an important food for metabolism since it is shelf stable, compact, and easily transported. I will update this post with candies that are found to have ingredients favorable for metabolism. If you know of such candies, please post them here.

Hard Candies:

Gummy Candies:
[Image: Gold-Bears_NEW_0_0_180_355_7701.png] Haribo Gold-Bears, ingredients: Corn Syrup, Sugar, Gelatin, Dextrose, Citric Acid, Corn Starch, Artificial and Natural Flavors, Fractionated Coconut Oil, Carnauba Wax, Beeswax Coating, Artificial Colors: Yellow No. 5, Red No. 40, Blue No. 1.

Chocolate Products:

[Image: 1509_Theo_ClassicBars_45Milk_Web_CL_%402x.jpg]  Organic Theo Milk Chocolate, ingredients: Cane Sugar, Cocoa Beans, Cocoa Butter, Milk Powder, Ground Vanilla Bean
by Sea at 04-27-2016, 12:05 AM
Review products or make recommendations from a metabolic point of view.
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