What would a 55y/o be CRAZY not to take?
Brook Stevens
I could ask, "what supplements are you taking?" But many of you may be
taking supplements that you have a hunch are good, but which evidence is
lacking. So, I'm wondering, if you had to pick the supplements that have
solid evidence that they are good for health and/or longevity, what would
those be? (Let's ignore diet and lifestyle - not that they aren't
important.)
Here's my list:
Natural beta-carotene/mixed carotenoids
C
D3
Vitamin K
Vitamin E (Mixed tocopherols with high Gamma E)
Tocotrienols
B1
B2
B3
B6 (Pyridoxamine)
Folic Acid
B12 (Methylcobalamin)
Biotin
B5
Calcium (Citrate, Citrate-Malate, or Glyconate)
Magnesium (Glyconate or Taurinate)
Zinc
Selenium
Chromium (Polynicotinate, etc.)
N-acetyl-Cysteine
Taurine
Arginine
Acetyl-L-Carnitine
R-Lipoic Acid
Resveratrol
Curcumin
Green Tea
Fish Oil
What's your list?
tcar...@elp.rr.com
Good job of picking out the best tasting, low hanging fruit. I
would subtract nothing but add;
Melatonin
Ginkoe biloba
Garlic
CoQ10
Milk thistle
and lycopene if 20 mg were not included in the carotenoids.
Thomas
Michael C Price
news:BEB6339F.2FC40%br...@nospam.com...
>
> What's your list?
>
My list is:
Daily, divided over meals, I take:
Approximately the "recommended" dose(~10 tablets/d) of Life Extension Mix +
Booster (which contains a general mixture of vitamins, minerals and
phytochemicals) plus extra B-vitamins and others. Some of the amounts are
more than optimal since they come from complexes.
This includes:
B-vitamins:
Thiamine (B1), 825 mg
Riboflavin (B2), 400 mg
Niacin (B3), 1575 mg
Inositol (B8), 2000 mg
Inositol hexanicotinate, 2480mg niacin (B3), 400mg inositol(B8)
Pantothenate (B5), 7.6 gm
Pyridoxine (B6), 625 mg
Biotin (B7), 4.8 mg
Folate (B9), 8 mg
Cyano-cobalamin (B12), 7 mg
Methyl-cobalamin (B12), 6 mg
Choline (B4), 545 mg
PABA (B10), 900 mg
TMG, 450 mg
Minerals:
Boron, 9 mg
Chromium, 1200ug
Copper, 6 mg
Magnesium, 2000 mg
Manganese, 60 mg
Molybdenum, 750ug
Selenium, 800 ug, in various organic and inorganic forms
Vanadium, 22.5mg
Zinc, 95 mg
Acetyl-L-carnitine, 1000mg
Alpha-lipoic acid, 500mg
RNA, 1000 mg
Aspirin, 150 mg
Beta-carotene, 150,000 IU
Glucosamine, 1000 mg
Lycopene, 40 mg + other carotenoids
Saw palmetto, 1240 mg
Vitamin C, 3 gm
Vitamin D3, 2400 IU
Vitamin E, 600 IU
Vitamin K (18mg K1, 2mg K2)
I don't take any hormones, including DHEA, HGH or melatonin.
Cheers,
Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm
njnava...@yahoo.com
Depending on how much B3 you're taking, you may want to consider adding
some methyl donors to the list. (In fact you should probably add some
anyway).
Regards,
Nelson Navarro
Larry Sharp
valuable substance to include.
--
Posted via Mailgate.ORG Server - http://www.Mailgate.ORG
Olafur Pall Olafsson
njnava...@yahoo.com wrote:
> Hello,
>
> Depending on how much B3 you're taking, you may want to consider
adding
> some methyl donors to the list. (In fact you should probably add some
> anyway).
>
> Regards,
> Nelson Navarro
I agree with the consideration of adding methyl donors to the list but
am curious to know why you say it depends on how much B3 he's taking?
I know B6, B12, folic acid and TMG help with methylation but have never
heard of B3. Was this an error?
njnava...@yahoo.com
No it wasn't an error. Niacin (or niacinamide) metabolism requires
methyl groups. The methyl groups have to come from somewhere. This may
be why some people have liver problems when taking large doses of
niacin. If you're taking hundreds of mg of B3, it's probably a good
idea to take some TMG or choline (or lecithin).
Med Hypotheses. 2000 Sep;55(3):189-94. Related Articles, Links
Co-administration of equimolar doses of betaine may alleviate the
hepatotoxic risk associated with niacin therapy.
McCarty MF.
Pantox Laboratories, San Diego, California 92109, USA.
High-dose niacin has versatile and substantial efficacy for the
treatment of hyperlipidemias, but its utility is compromised by various
side effects, the most serious of which is liver damage. It is proposed
that this hepatotoxicity reflects the high demand for methyl groups
imposed by niacin catabolism, leading to a reduction in hepatic levels
of S-adenosylmethionine (SAM). Depletion of the hepatic SAM pool has
likewise been shown to mediate, at least in part, the hepatotoxic
effects of ethanol, methotrexate, and niacinamide. If niacin does
indeed decrease SAM, a likely consequence would be a counterproductive
elevation of plasma homocysteine. Conceivably, methyl group deficiency,
by altering membrane properties of skeletal muscle, also contributes to
niacin-induced insulin resistance. Concurrent betaine supplementation -
preferably administered as a complex with equimolar amounts of niacin -
may represent the most cost-effective way to prevent niacin-mediated
depletion of SAM and thus avoid hepatotoxicity (and possibly other
adverse effects) while controlling homocysteine. Betaine also merits
evaluation as an adjuvant to methotrexate and niacinamide therapies.
PMID: 10985907 [PubMed - indexed for MEDLINE]
Brook Stevens
> Hello,
>
> Depending on how much B3 you're taking, you may want to consider adding
> some methyl donors to the list. (In fact you should probably add some
> anyway).
>
> Regards,
> Nelson Navarro
Are you suggesting TMG? Or what else?
Brook Stevens
Thanks for the list. I should have had choline and inositol in my list. I
forgot. I agree with Aspirin too, and most of the rest of your list...
What does RNA do?
If I don't have BPH, do you still recommend Saw Palmetto?
Just curious, how do you not have diarrhea from 2gm of magnesium?
For reason's Paul Wakfer has listed, I don't think I want to take
Glucosamine if I don't have arthritis.
The reading I've done on Vanadium is that there is no benefit at doses
below... I forget, 100mg? 200mg? And those doses are thought to be toxic.
I've seen Vanadium Chelavite is now being sold and I wonder if that might be
less toxic.
One of my objectives here is that I can tell my doctor what I'm taking and
he won't yell at me. Or say things like:
"that's not proven to do anything"
"we don't know the long-term consequences are of taking..."
I agree with most of the things on your list, but I think my doctor would
freak out over many of the doses.
Brook
Brook Stevens
> In addition to all the other recommendations, Carnosine would be a
> valuable substance to include.
I'd love to get additional AGE breaking if Carnosine was shown to be okay to
take long-term. Others may be okay with it's risk-reward ratio, and level of
uncertainty. I posted earlier, I want to be able to defend my choices to my
doctor, and I don't see how I can defend this one. It might be great, but as
Michael C Price wrote, your body has enzymes (or something) to break down
Carnosine -- so it seems like it must be a negative somewhere, somehow. Even
though your body makes it and uses it and levels go down as you age.. still,
how much is okay to take every day for 20 years? I don't know. Do you know?
Brook
Michael C Price
Gets digested and broken down into a number of coenzymes for
ribozymes (enzymes made from nucleic acids instead of animo acids).
In health terms, seems to boost the immune system and
who-knows-what-else.
> If I don't have BPH, do you still recommend Saw Palmetto?
Well, *I* would take saw palmetto even if I didn't have BPH.
My self-diagnosis is that had BPH from my early 20s, but that
S-P has reversed it. And largely halted the progression of early
baldness that started -- can you believe it -- in my teens :-(
> Just curious, how do you not have diarrhea from 2gm of magnesium?
I am naturally constipated -- the magnesium restores me to normalacy.
2gm may be too much for most people, but it's okay for me.
> For reason's Paul Wakfer has listed, I don't think I want to take
> Glucosamine if I don't have arthritis.
That's fine if you don't have arthritis -- but I do (or would have
if I didn't take glucosamine). My non-supplementing brother
(same age: 45) has early stage arthritis -- all his joints start to
sieze up unless he keeps moving. I up my dose when warning signs
develop and for as long as they persist; all I can say is that it works
wonders for me.
> The reading I've done on Vanadium is that there is no benefit at doses
> below... I forget, 100mg? 200mg? And those doses are thought to be toxic.
Weight trainers and athletes often take 60mg (PMID: 10382561), so I
presume there is some benefit at that dose. Plus the sulfate form seems
safe at that level (again, PMID: 10382561) or even higher levels
(PMID: 10497891).
Refs at end.
>
> I've seen Vanadium Chelavite is now being sold and I wonder if that
> might be less toxic.
>
>
> One of my objectives here is that I can tell my doctor what I'm taking
> and he won't yell at me. Or say things like:
>
> "that's not proven to do anything"
> "we don't know the long-term consequences are of taking..."
>
> I agree with most of the things on your list, but I think my doctor
> would freak out over many of the doses.
I'm sure he would. I'm sure my doctor would also -- if I had one.
Cheers,
Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm
Mol Cell Biochem. 1999 Aug;198(1-2):157-61.
Effect of oral vanadyl sulfate treatment on serum enzymes and lipids of
streptozotocin-diabetic young rats.
Pepato MT, Magnani MR, Kettelhut IC, Brunetti IL.
Department of Clinical Analysis, Faculty of Pharmaceutical Sciences of
Araraquara, UNESP, SP, Brazil.
In this work we investigate the possible toxicity of vanadyl sulfate
(VOSO4), a compound capable of reducing hyperglycemia, on the following
serum enzymes of diabetic young rats: alanine aminotransferase (ALT),
aspartate aminotransferase (AST), lactate dehydrogenase (LD) and creatine
kinase (CK), as well as its effects on serum lipids. We find that at a
concentration of 1 mg/mL VOSO4 has no toxic effect on the liver and muscles
of diabetics young rats. These findings suggest that VOSO4 may be an
alternative to insulin in the near future, due to its low cost, low toxicity
and ready availability.
PMID: 10497891
J Toxicol Clin Toxicol. 1999;37(2):265-78.
Erratum in:
J Toxicol Clin Toxicol 2000;38(7):813.
Vanadium.
Barceloux DG.
Vanadium is a steel-grey, corrosion-resistant metal, which exists in
oxidation states ranging from -1 to +5. Metallic vanadium does not occur in
nature, and the most common valence states are +3, +4, and +5. The
pentavalent form (VO3-) predominates in extracellular body fluids whereas
the quadrivalent form (VO+2) is the most common intracellular form. Because
of its hardness and its ability to form alloys, vanadium (i.e.,
ferrovanadium) is a common component of hard steel alloys used in machines
and tools. Although most foods contain low concentrations of vanadium (< 1
ng/g), food is the major source of exposure to vanadium for the general
population. High air concentrations of vanadium occur in the occupation
setting during boiler-cleaning operations as a result of the presence of
vanadium oxides in the dust. The lungs absorb soluble vanadium compounds
(V2O5) well, but the absorption of vanadium salts from the gastrointestinal
tract is poor. The excretion of vanadium by the kidneys is rapid with a
biological half-life of 20-40 hours in the urine. Vanadium is probably an
essential trace element, but a vanadium-deficiency disease has not been
identified in humans. The estimated daily intake of the US population ranges
from 10-60 micrograms V. Vanadyl sulfate is a common supplement used to
enhance weight training in athletes at doses up to 60 mg/d. In vitro and
animal studies indicate that vanadate and other vanadium compounds increase
glucose transport activity and improve glucose metabolism. In general, the
toxicity of vanadium compounds is low. Pentavalent compounds are the most
toxic and the toxicity of vanadium compounds usually increases as the
valence increases. Most of the toxic effects of vanadium compounds result
from local irritation of the eyes and upper respiratory tract rather than
systemic toxicity. The only clearly documented effect of exposure to
vanadium dust is upper respiratory tract irritation characterized by
rhinitis, wheezing, nasal hemorrhage, conjunctivitis, cough, sore throat,
and chest pain. Case studies have described the onset of asthma after heavy
exposure to vanadium compounds, but clinical studies to date have not
detected an increased prevalence of asthma in workers exposed to vanadium.
Publication Types:
Review
Review, Tutorial
PMID: 10382561
Michael C Price
> [RNA] gets digested and broken down into a number of
> coenzymes for ribozymes (enzymes made from nucleic acids
> instead of animo acids)
I should have added "and conventional enzymes (made from
amino acids)".
RNA gets broken down and converted into coenzymes --
the most important of which are ATP, CTP, UTP & GTP,
which supply energy for numerous reactions. This degrades
the tri-phosphates to di- or mono-phosphates before being
converted back to their tri-phosphate forms.
Here's what my files say:
During digestion RNA is broken down into, and absorbed as, nucleotides and
nucleosides. Nucleotides and nucleosides have a direct metabolic action,
independent of their role in RNA, being the precursors to a number of
coenzymes. The energy-supplying coenzyme ATP is a nucleotide, for instance,
critical to our metabolism. There are other nucleotide coenzymes, such as
UDP and CDP, required for biosynthesis of glycosaminoglycans, lipids and
glycogen. (NAD and CoA are also nucleotide coenzymes, but are not derived
from dietary nucleic acids.) Ribozymes, enzymes constructed from
nucleotides instead of amino acids, are another example of the role of
nucleotides.
RNA has a high turnover, being required for all gene expression and protein
synthesis. We are capable of synthesising nucleotides from scratch (via the
de novo pathways) but this is very expensive, in terms of the energy
required. To ease the burden of de novo synthesis we have evolved the
so-called salvage pathways which process nucleotides & nucleosides available
both from our diet and from the natural turnover and breakdown of cellular
RNA.
The amount of RNA in foodstuffs varies widely. Sardines, one of the most
RNA rich foods, are between 0.5% - 1% by weight. To ingest the 250mg of RNA
required for the life extension effect, we need only eat 12 - 25 g of
sardines per day; even less of chlorella.
Summary: RNA enriched diets are beneficial to health, and in particular the
immune system and have extended lifespan
Some terms:
Coenzyme - a coenzyme is a complex molecule that an enzyme requires in order
to function. A coenzyme either bonds permanently onto the enzyme, forming a
prosthetic group, or is required as a co-substrate by the enzyme.
Apoenzymes, with the exceptions of ribozymes, are proteins constructed from
amino-acids. This limits the range of their flexibility or activity. The
coenzymes, by contrast, are not amino-acid based, and supply the more
diverse arrangements of molecules that apoenzymes require to complete their
structure and function correctly as holoenzymes. In general a particular
coenzyme performs one just biochemical action, but enzymes and coenzymes
have a many-to-many relationship; a particular coenzyme is typically
required by a number, sometimes hundreds, of different enzymes and,
conversely, one enzyme may require the presence of many coenzymes to
function.
Ribozyme - A small number of important non-proteonomic enzymes are formed
from nucleotides, not amino acids. Ribozymes are believed to be the most
ancient of all enzymes, evolving before the now more numerous proteonomic
enzymes, and still play a pivotal role in metabolism. Telomerase is a
ribozyme.
Manfred Bartz
> I'd love to get additional AGE breaking if Carnosine was shown to be
> okay to take long-term. Others may be okay with it's risk-reward
> ratio, and level of uncertainty. I posted earlier, I want to be able
> to defend my choices to my doctor, and I don't see how I can defend
> this one. ...
> ... It might be great, but as Michael C Price wrote, your body
> has enzymes (or something) to break down Carnosine -- ...
Yes.
From <http://www.reflex-nutrition.com/glossary/#L-Carnosine>:
L-Carnosine is comprised of two amino acids, histidine and
beta-alanine, and is termed a di-peptide. L-Carnosine's role in
the body diverse and pro-found, it is found naturally in muscles,
brain, liver and other vital tissues.
Both, L-Histidine and L-Alanine are genetically coded amino acids.
Chains of amino acids are called peptides if they are short, and they
are called proteins if they are long. The cutoff between the
definitions is somewhere between 50 and 100 amino acids in the chain.
Our digestive system is designed to use digestive enzymes to
disassemble chains of amino acids (proteins, peptides) and absorb the
individual amino acids. Latest research shows that the disassembly is
not always perfect and short peptides can get absorbed too. (Sorry,
have not got a reference handy)
> ... so it seems
> like it must be a negative somewhere, somehow.
I don't see any reason why there "must be a negative somewhere,
somehow" ... ;-)
My guess is that some of the orally taken carnosine will be broken up
into its amino acids and some will be absorbed intact. Since
carnosine as well as the individual amino acids are naturally occuring
building blocks of our bodies I don't see any potential for harm.
You eat some protein, don't you?
Cheers
--
Manfred Bartz (I am not a doctor...)
rs1...@techemail.com
Carnosinase does not exist primarily to break down carnosine; it exists
in order to lead to the production of histidine and alanine. When this
argument came up before, someone used the analogy of carotenase
breaking down carotene into vitamin A. When the enzyme is lacking
altogether, upregulation of carnosine production occurs in a desperate
attempt to derive more histidine and alanine (carnosinemia). It used
to be thought that excess carnosine itself caused the condition, but
one case report told of a patient who showed improvement after
injections of histidine and alanine, after which carnosine levels went
down. Carnosinase may have a secondary function of breaking down
oxidized carnosine. Carnosine is continuously produced in modest
amounts in the body in order to satisfy the need for a constand supply
of histidine and alanine, and this also may function indirectly as a
way to keep a supply of unoxidized carnosine available.... although
this is just a personal hypothesis.
Michael C Price
Interesting. Can you give a reference for this hypothesis
(the case study, for example)?
Olafur Pall Olafsson
Brook Stevens wrote:
> Larry Sharp on 5/23/05 1:15 PM wrote:
>
> > In addition to all the other recommendations, Carnosine would be a
> > valuable substance to include.
>
> I'd love to get additional AGE breaking if Carnosine was shown to be okay to
> take long-term. Others may be okay with it's risk-reward ratio, and level of
> uncertainty.
First of all Carnosine does not break AGE's it only prevents their
formation.
And low doses of Carnosine are probably very safe in the long term
because people get Carnosine in low doses from food. People get on
average about 50-250mg of Carnosine daily from their diet. I don't
have any references but I recall that you have to take a bit higher
amount than 500mg of Carnosine a day to reach the limit of the
Carnosinase enzyme and raise Carnosine levels in the body. For this
reason 500mg or less of Carnosine a day is probably very safe. But
this might depend somewhat on the condition of your liver according to
the abstract below.
Clin Chem. 1986 Aug;32(8):1563-5. Related Articles, Links
Decreased activity of carnosinase in serum of patients with chronic
liver disorders.
Bando K, Ichihara K, Toyoshima H, Shimotuji T, Koda K, Hayashi C, Miyai
K.
We measured the activity of carnosinase, a prominent hepatic peptidase,
in sera from 69 patients with liver disorders. Mean values (and SDs)
for those with liver cirrhosis (17 cases) and hepatoma (seven cases)
were 0.51 (0.28) and 0.68 (0.21) mumol/mL per hour,
respectively--clearly less than for normal adults: 4.19 (0.95) mumol/mL
per hour. Samples from 17 cases of chronic hepatitis also showed
moderately decreased activity, 1.41 (0.97) mumol/mL per hour. In
contrast, 14 cases of acute hepatitis generally showed values falling
within the normal limits: 3.41 (1.97) mumol/mL per hour. Our results
for carnosinase correlated with those for cholinesterase (r = 0.70) and
with the concentration of albumin in serum (r = 0.59), but not with the
activity of either creatine kinase, aspartate aminotransferase, or
alanine aminotransferase in serum. Carnosinase values differed more
among groups of disorders than did the values for cholinesterase or
albumin. Measurement of serum carnosinase activity may be of clinical
value in assessing the severity of chronic liver-cell damage, but not
in differentiating liver disease from nutritional, muscle, or endocrine
disorders.
PMID: 3731453 [PubMed - indexed for MEDLINE]
And you don't necessarily have to raise the level of Carnosine in the
body to get antiglycation effects from taking it. Some of the
antiglycation effects of Carnosine in the body are derived from it's
breakdown products. Histidine seems to be particularily effective as
an antiglycative agent according to the abstract below.
Life Sci. 2004 Jul 30;75(11):1379-89. Related Articles, Links
Anti-crosslinking properties of carnosine: significance of histidine.
Hobart LJ, Seibel I, Yeargans GS, Seidler NW.
Department of Biochemistry, University of Health Sciences, 1750
Independence Avenue, Kansas City, MO 64106-1453, USA.
Carnosine, a histidine-containing dipeptide, is a potential treatment
for Alzheimer's disease. There is evidence that carnosine prevents
oxidation and glycation, both of which contribute to the crosslinking
of proteins; and protein crosslinking promotes beta-amyloid plaque
formation. It was previously shown that carnosine has anti-crosslinking
activity, but it is not known which of the chemical constituents are
responsible. We tested the individual amino acids in carnosine
(beta-alanine, histidine) as well as modified forms of histidine
(alpha-acetyl-histidine, 1-methyl-histidine) and methylated carnosine
(anserine) using glycation-induced crosslinking of cytosolic aspartate
aminotransferase as our model. beta-Alanine showed anti-crosslinking
activity but less than that of carnosine, suggesting that the
beta-amino group is required in preventing protein crosslinking.
Interestingly, histidine, which has both alpha-amino and imidazolium
groups, was more effective than carnosine. Acetylation of histidine's
alpha-amino group or methylation of its imidazolium group abolished
anti-crosslinking activity. Furthermore, methylation of carnosine's
imidazolium group decreased its anti-crosslinking activity. The results
suggest that histidine is the representative structure for an
anti-crosslinking agent, containing the necessary functional groups for
optimal protection against crosslinking agents. We propose that the
imidazolium group of histidine or carnosine may stabilize adducts
formed at the primary amino group.
PMID: 15234195 [PubMed - indexed for MEDLINE]
beni
beni.
Olafur Pall Olafsson
beni wrote:
> So how much histidine to take?
> beni.
Hi beni,
I don't know if supplementing with histidine is such a good idea.
Histidine can be converted to histamine in the body which can cause
allergic reactions. However since you already get about 1-3 grams of
histidine for every 100g of protein you eat daily supplementing with
low amounts of it, maybe a gram a day or less, should be very safe.
Another way is to simply take low doses of carnosine which will then be
converted to histidine and beta-Alanine both of which seem to have some
antiglycative effects.
I personally just take 500mg of Carnosine daily. This is a very safe
amount because it's probably not high enough to override the
Carnosinase enzyme, but it should give me some antiglycative benefits.