 |
Gout
is an arthritis-like condition that occurs when there is too
much uric acid present in the bloodstream. When this happens,
joint inflammation occurs, followed by intense joint pain.
Symptoms of gout are caused by elevated levels of uric acid
in the blood which crystallize and are deposited in joints,
tendons, and surrounding tissues.
A positive diagnosis for gout is confirmed clinically by the
visualization of the characteristic crystals in joint fluid.
If the diagnosis is in doubt, synovial fluid analysis should
be conducted.
Hyperuricemia is the underlying cause of gout, which can occur
for a number of reasons, including genetic predisposition,
diet, or underexcretion of urate (the salts of uric acid).
Gout is mostly found in overweight men over the age of 35.
|
GOUT
THE
GLYCEMIC INDEX, COFFEE & TEA
|
The relationship between
incidence of gout and consumption of high glycemic sugars,
and the relationship between gout and coffee and tea, has
been researched and published in peer-reviewed journals.
There are two very different effects related to the ingestion
of high glycemic sugars, and the ingestion of coffee and tea
on the condition of gout:
| • |
High glycemic sugars elevate risk of gout and worsen
symptoms, while low glycemic sugars and ingredients
do not cause this effect |
| •
|
Coffee
& tea have proven benefits |
In this report, we will discuss and
identify the clinical relationship between:
| •
|
Gout and ingestion of high glycemic
sugars |
| •
|
Gout
and ingestion of coffee and tea |
|
INGESTION
OF HIGH GLYCEMIC SUGARS
& PRODUCTS ARE RELATED TO GOUT
|
High
glycemic ingredients elevate insulin levels (insulinogenic)
in humans, which is a very negative metabolic event, leading
to weight gain, obesity, shortened lifespan, and increased
risk of gout.
Because of the relationship between high glycemic sugars and
insulin-response, consuming high glycemic insulinogenic beverages,
foods, and Nutraceuticals, exacerbates (worsens) the condition
of gout, and greatly elevates the risk of developing gout.
Sugars and ingredients that elevate blood glucose (high glycemic)
levels include sucrose (table sugar), honey, maltose, maltodextrins,
and high-fructose corn syrup. The list of other known high
glycemic sweeteners, sugars, and ingredients is quite extensive
and spans 27-years of research (Glycemic Research
Institute / Comprehensive List of Sugars / Sweeteners).
|
The
mechanism by which insulinogenic ingredients worsen and
increase risk of gout:
|
| •
|
Ingestion of
insulinogenic sugars prevents the excretion of uric acid from
the body |
| •
|
As
the concentration of uric acid in the body increases, uric
acid in the joint liquid increases, causing the uric acid
to precipitate into crystals |
| •
|
High uric acid levels
are a known precursor of gout |
COFFEE
PROVEN BENEFICIAL IN DECREASING RISK & INCIDENCE OF GOUT
JOURNAL
OF ARTHRITIS CARE
& RESEARCH
|
A
large-scale study published in the journal Arthritis
Care & Research (1) examined the relationship
between coffee, tea, caffeine intake.
Coffee is one of the most widely consumed beverages in the
world, and more than 50 percent of Americans drink
it at the average rate of 2 cups per day.
Because of this widespread consumption, coffee’s potential
effects have important implications for public and individual
health.
The study, led by Hyon K. Choi, University of British Columbia
in Vancouver, Canada, included over 14,000 men and women,
at least 20 years old, who consented to a medical exam in
which blood and urine specimens were obtained.
Results of the peer-reviewed
published trial showed that:
|
| • |
Coffee
is beneficial in decreasing risk and incidence of gout in
humans |
| • |
4
cups of coffee per day lowers uric acid levels, attributed
to the natural polyphenols found in coffee |
| • |
High
uric acid levels in the blood are a precursor of gout, the
most common inflammatory arthritis in adult men |
| • |
Coffee
consumption is associated with lower uric acid levels, which
appears to be due to natural phytochemicals other than caffeine |
| • |
The
results showed that levels of uric acid in the blood significantly
decreased with increasing coffee intake, but not with tea
intake |
| • |
The
risk of gout was 40 percent lower for men who drank 4 to 5
cups a day and 59 percent lower for men who drank 6 or more
cups a day than for men who never drank coffee |
| • |
There
was no beneficial association between total caffeine intake
from beverages and uric acid levels |
LONG-TERM
STUDY OF COFFEE & GOUT:
AMERICAL JOURNAL OF
CLINICAL NUTRITION
|
The
Arthritis Care & Research study
was independently validated and published in the American
Journal of Clinical Nutrition (2) in 2010.
Researchers examined the relationship between coffee intake
and incidence of gout in a large subject group of 89,433 female
humans over a 26-year period. The study included the consumption
of coffee, decaffeinated coffee, tea, and total caffeine.
The research project determined that “Long-term coffee consumption
is associated with a lower risk of incident gout in women.”
This data is consistent with the findings reported in the
journal of Arthritis Care & Research.
|
COFFEE
DECREASES URIC ACID LEVELS
JOURNAL OF ARTHRITIS
and RHEUMATISM |
The journal of Arthritis and Rheumatism
(3) reported that, in both men and women, “Serum uric acid
levels decrease with increasing coffee intake.”
Researchers studied data from 14,758 men and women, and
examined the relationship between coffee, tea, and caffeine
intake and serum uric acid level using linear regression.
Additionally, they examined the relationship with hyperuricemia
(serum uric acid >7.0 mg/dl among men and >5.7 mg/dl
among women) using logistic regression.
CONCLUSIONS:
|
| • |
Coffee consumption is associated with lower serum uric acid
level and hyperuricemia frequency, but tea consumption is
not. |
| • |
The
inverse association with coffee appears to be via components
of coffee other than caffeine |
 |
 |
According
to the researchers, the variable between the gout-reducing
effects of coffee versus tea appear to be related to the components
of coffee. Coffee contains a vast amount of natural
phytochemicals other than caffeine.
One specific component of tea has been identified by researchers
as a potential nutritional adjunct in the treatment of gout
(4).
Epigallo catechin-O-gallate (EGCG), the most active epicatechin
in green tea was identified by researchers as “A potent inducer
of apoptosis and an inhibitor of telomerase activity” and
an anti-oxidant that provides reduction of inflammatory
processes (High uric acid levels in the blood are a precursor
of gout, the most common inflammatory arthritis in adult men).
In humans, EGCG acts on different processes, and triggers
various molecular mechanisms of action.
According to researchers, tea does not appear to effect gout
either positively or negatively, while EGCG (from green tea)
may positively support nutritional intervention related to
incidence of gout.
|
 |
LOW-FAT
DAIRY PRODUCTS
DECREASE RISK OF GOUT |
 |
The
New England Journal of Medicine
(5) published a trial that followed 47,150 males over a 12-year
period, to determine risk and causes of gout.
The research team followed 47,150 men with no prior history
of gout over a 12-year period. During the 12-year period,
730 men were diagnosed with gout.
Study participants who consumed the highest amount of meat
were 40 percent more likely to have gout than those who ate
the least amount of meat and study participants who ate the
most seafood were 50 percent more likely to develop gout.
The researchers also reported that:
| • |
Low-fat dairy products decreased the risk of gout
|
| • |
“The
incidence of gout decreased with increasing intake
of [low-fat] dairy products.” |
| • |
“Furthermore,
we found a strong inverse association between the
consumption of dairy products, especially low-fat
dairy products, and the incidence of gout.” |
In regards to incidence of gout and low-fat dairy intake,
the researchers stated “The multivariate relative risk of
gout among men in the highest quintile of dairy intake, as
compared with those in the lowest quintile, was 0.56 (95 percent
confidence interval, 0.42 to 0.74; P for trend <0.001).”
|
 |
GOUT:
CAUSAL FACTORS
Contributing
factors related to the
development of gout include:
|
| • |
Heredity:
Genetics contributes to 60% of variability in uric acid levels)
|
| • |
Consumption
of alcoholic or soft drink beverages on a daily basis |
| • |
Smoking |
| • |
Regular
use of medications such as aspirin |
| • |
Poor
diet |
| • |
High-protein
diets, such as the Atkins diet |
| • |
Metabolic
Syndrome and/or Obesity:
A body mass index greater than or equal to 35 increases a
male's risk of gout threefold
The combination of abdominal obesity, hypertension, insulin
resistance and abnormal lipid levels occurs in nearly 75%
of all gout cases |
| • |
Chronic
lead exposure and lead-contaminated alcohol are risk factors
for gout due to the harmful effect of lead on kidney function |
| • |
Gout
may be secondary to sleep apnea via the release of purines
from oxygen-starved cells - Treatment of sleep apnea can lessen
the occurrence of gout attacks |
| • |
Fasting
and/or severe dieting can raise uric acid levels and cause
gout to worsen |
Foods
most likely to cause gout/exacerbate gout:
|
| • |
Red
meats, seafood and poultry:
Study participants who consumed the highest amount of meat
were 40 percent more likely to have gout than those who ate
the least amount of meat.
Study participants who ate the most seafood were 50 percent
more likely to have gout. |
| • |
Drinks
most likely to cause gout include alcoholic beverages, especially
beer, wine and soda. |
Foods
that help prevent gout:
|
| • |
Coffee, vitamin C and low-fat dairy products decrease risk
of gout |
| • |
Physical
fitness appear to decrease the risk of gout |
| • |
Vegetables
(even high-purine veggies) such as: peas, beans, mushrooms,
cauliflower, spinach |
Drinking
the daily recommended dose of water is the best prevention
of gout because water can help remove uric acid from the body.
Aim for eight to sixteen 8-ounce (237 milliliter) glasses
a day. |
The
Boresha Medical Advisory Board strives to integrate
current valid research into its product line, and to update
products based on important new findings in the field of nutrition,
obesity, diabetes, and anti-aging. |
| • |
Boresha’s
B-Skinny Coffee and Nuvo Gene Tea™ are based on 27-years of
research, and reflect current scientific evidence and protocols
for safe and efficacious Thermogenic Nutraceuticals |
| • |
Boresha
products do not contain any High Glycemic ingredients, and
are Certified Low Glycemic |
| • |
Boresha’s
B-Creamy coffee-creamer is a -0- Fat, 100% natural dairy product |
| • |
B-Sweet
is a completely natural Low Glycemic, Diabetic Friendly fruit
sweetener backed by years of clinical trials |
| • |
The
molecule EGCG is a vital ingredient in Boresha’s Nuvo Gene
Tea™ |
Copyright®
November 2010-Updated: July 2011
No copies of this
article may be made or distributed
without prior written permission from the authors.
|
 |
 |
 |
(1)
“Coffee, Tea, and Caffeine Consumption and Serum Uric Acid
Level: The Third National Health and Nutrition Examination
Survey,” Hyon K. Choi, Gary Curhan, Arthritis Care & Research,
June 2007; 57:5
(2) Coffee consumption and risk of incident gout in women:
the Nurses' Health Study. American Journal of Clinical Nutrition;
Am J Clin Nutr. 2010 Oct;92(4):922-7.
(3) Journal of Arthritis and Rheumatism; Arthritis Rheum.
2007 Jun 15;57(5):816-21.
(4) Bullitin Du Cancer. 1999 Sep;86(9):721-4. Multiple actions
of EGCG, the main component of green tea.
(5) Purine-Rich Foods, Dairy and Protein Intake, and the Risk
of Gout in Men. New England Journal of Medicine; Volume 350:1093-1103,
March 11, 2004.
Dohan, J. L., Schlesinger, N., Choi, H. K., Curhan, G. (2004).
Purine-Rich Foods and the Risk of Gout in Men. NEJM 350: 2520-2521
Roubenoff R, Klag MJ, Mead LA, Liang KY, Seidler AJ, Hochberg
MC. Incidence and risk factors for gout in white men. JAMA
1991;266:3004-3007.
Emmerson BT. The management of gout. N Engl J Med 1996;334:445-451.
Gibson T, Rodgers AV, Simmonds HA, Court-Brown F, Todd E,
Meilton V. A controlled study of diet in patients with gout.
Ann Rheum Dis 1983;42:123-127.
Matzkies F, Berg G, Madl H. The uricosuric action of protein
in man. Adv Exp Med Biol 1980;122:227-231.
Garrel DR, Verdy M, PetitClerc C, Martin C, Brule D, Hamet
P. Milk- and soy-protein ingestion: acute effect on serum
uric acid concentration. Am J Clin Nutr 1991;53:665-669.
Ghadirian P, Shatenstein B, Verdy M, Hamet P. The influence
of dairy products on plasma uric acid in women. Eur J Epidemiol
1995;11:275-281.
Wallace SL, Robinson H, Masi AT, Decker JL, McCarty DJ, Yu
TF. Preliminary criteria for the classification of the acute
arthritis of primary gout. Arthritis Rheum 1977;20:895-900.
Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and
the risk of coronary heart disease in women. N Engl J Med
1997;337:1491-1499.
Clifford AJ, Riumallo JA, Young VR, Scrimshaw NS. Effect of
oral purines on serum and urinary uric acid of normal, hyperuricemic
and gouty humans. J Nutr 1976;106:428-434.
Lewis HB, Doisy EA. Studies in uric acid metabolism. I. The
influence of high protein diets on the endogenous uric acid
elimination. J Biol Chem 1918;36:1-7.
Raiziss GW, Dubin H, Ringer AI. Studies in endogenous uric
acid metabolism. J Biol Chem 1914;19:473-485.
Dessein PH, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J.
Beneficial effects of weight loss associated with moderate
calorie/carbohydrate restriction, and increased proportional
intake of protein and unsaturated fat on serum urate and lipoprotein
levels in gout: a pilot study. Ann Rheum Dis 2000;59:539-543.
Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. Effect
of low level lead exposure on hyperuricemia and gout among
middle aged and elderly men: the Normative Aging Study. J
Rheumatol 2000;27:1708-1712.
Sharpe CR. A case-control study of alcohol consumption and
drinking behaviour in patients with acute gout. Can Med Assoc
J 1984;131:563-567.
Zollner N. Influence of various purines on uric acid metabolism.
Bibl Nutr Dieta 1973;19:34-43.
Zollner N, Griebsch A. Diet and gout. Adv Exp Med Biol 1974;41:435-442.
Griebsch A, Zollner N. Effect of ribomononucleotides given
orally on uric acid production in man. Adv Exp Med Biol 1974;41:443-449.
Jordan,
K. M., Cameron, J. S., Snaith, M., Zhang, W., Doherty, M.,
Seckl, J., Hingorani, A., Jaques, R., Nuki, G., on behalf
of the British Society for Rheumatology, (2007). British Society
for Rheumatology and British Health Professionals in Rheumatology
Guideline for the Management of Gout. Rheumatology (Oxford)
46: 1372-1374
Sutaria, S., Katbamna, R., Underwood, M. (2006). Effectiveness
of interventions for the treatment of acute and prevention
of recurrent gout--a systematic review. Rheumatology (Oxford)
45: 1422-1431
Harrold, L R, Yood, R A, Mikuls, T R, Andrade, S E, Davis,
J, Fuller, J, Chan, K A, Roblin, D, Raebel, M A, Von Worley,
A, Platt, R, Saag, K G (2006). Sex differences in gout epidemiology:
evaluation and treatment. Ann Rheum Dis 65: 1368-1372
Zhang, W, Doherty, M, Pascual, E, Bardin, T, Barskova, V,
Conaghan, P, Gerster, J, Jacobs, J, Leeb, B, Liote, F, McCarthy,
G, Netter, P, Nuki, G, Perez-Ruiz, F, Pignone, A, Pimentao,
J, Punzi, L, Roddy, E, Uhlig, T, Zimmermann-Gorska, I (2006).
EULAR evidence based recommendations for gout. Part I: Diagnosis.
Report of a task force of the standing committee for international
clinical studies including therapeutics (ESCISIT). Ann Rheum
Dis 65: 1301-1311
Underwood, M. (2006). Diagnosis and management of gout.. BMJ
332: 1315-1319
Choi, H. K., Mount, D. B., Reginato, A. M. (2005). Pathogenesis
of Gout. ANN INTERN MED 143: 499-516
Suresh, E (2005). Diagnosis and management of gout: a rational
approach. Postgrad. Med. J. 81: 572-579 Snaith, M. (2004).
Gout and alcohol. Rheumatology (Oxford) 43: 1208-1209
Roubenoff R. Gout and hyperuricemia. Rheum Dis Clin North
Am 1990;16:539-550.
Glynn RJ, Campion EW, Silbert JE. Trends in serum uric acid
levels 1961-1980. Arthritis Rheum 1983;26:87-93.
|
|
 |
|