Glucosamine is an important building block needed by the body to manufacture specialized
molecules called glycosaminoglycans, found in cartilage.
Where is it found?
Glucosamine is not present in significant amounts in most diets. Supplemental sources are
derived from the shells of shrimp, lobster, and crab, or may be synthesized.
Glucosamine has been used
in connection with the following conditions (refer to the individual
health concern for complete information):
Who is likely to be deficient?
A glucosamine deficiency in humans has not been reported.
Which form is best?
Glucosamine is available in several forms. The glucosamine sulfate (GS) form (stabilized
with a mineral salt) is the only form clearly shown in clinical trials to be effective for osteoarthritis. For this reason, it is the
GS is stabilized with one of two mineral salts: sodium chloride (NaCl) or potassium
chloride (KCl).1 2 Although they both appear to effectively stabilize
GS, the use of KCl as a stabilizer seems preferable since the average Western diet already
provides far too much salt (NaCl) and not enough
potassium. However, most of the research has been done with the NaCl-stabilized form.
Concerns have been raised about the quality of GS products on the market. In one study, the
amount of glucosamine contained in 14 commercially available glucosamine products varied from
41% to 108% of the amount stated on the label.3 Even when the weight of the sulfate
molecule was included, 11 of the 14 products contained less than the amount of glucosamine
stated on the label. Some manufacturers may include the weight of the stabilizing salts (NaCl
or KCl) in the total weight of the product, without stating so on the label.
Glucosamine hydrochloride (GH) has been widely available as a dietary supplement for years,
but only one trial has evaluated this form of glucosamine as a single remedy for
OA.4 This trial found only minor significant benefits from 1,500 mg per day of GH
for eight weeks, in people with osteoarthritis of the knee who were also taking up to 4,000 mg
per day of acetaminophen. To more fairly
evaluate the effects of GH, future research should involve people not taking pain-relieving
Another form of glucosamine,
N-acetyl-glucosamine (NAG), has not been studied in people with osteoarthritis.
How much is usually taken?
Healthy people do not need to routinely supplement with glucosamine. Most research with
people who have osteoarthritis, uses 500 mg
three times per day of GS. Appropriate amounts for other conditions are not known.
Are there any side effects or interactions?
At the amount most frequently taken by adults—500 mg three times per day of
GS—adverse effects have been limited to mild reversible gastrointestinal side effects.
In one trial, people with peptic ulcers and
those taking diuretic drugs were more likely
to experience side effects.5
Animal research has raised the possibility that glucosamine could contribute to insulin resistance.6 7 This
effect might theoretically result from the ability of glucosamine to interfere with an enzyme needed to regulate blood sugar
levels.8 However, available evidence does not suggest that taking glucosamine
supplements will trigger or aggravate insulin resistance or high blood sugar.9 Two large, 3-year
controlled trials found that people taking GS had either slightly lower blood glucose
levels or no change in blood sugar levels, compared with people taking placebo.10
11 Until more is known, people taking glucosamine supplements for long periods may
wish to have their blood sugar levels checked; people with diabetes should consult with a doctor before taking
glucosamine and should have blood sugar levels monitored if they are taking glucosamine.
In 1999 the first case of an allergic
reaction to oral GS was reported.12 Allergic reactions to this supplement
appear to be rare.
Some GS is processed with sodium chloride (table salt), which is restricted in some diets
(particularly for people with high blood
The theory that GS and chondroitin sulfate
work synergistically in the treatment of
osteoarthritis remains unproven.
At the time of writing, there were no well-known drug interactions
1. Drovanti A, Bignamini AA, Rovati AL. Therapeutic activity of oral
glucosamine sulfate in osteoarthritis: a placebocontrolled doubleblind
investigation. Clin Ther 1980;3:260–72.
2. Vaz AL. Doubleblind clinical evaluation of the relative efficacy
of ibuprofen and glucosamine sulphate in the management of osteoarthritis of the knee in
outpatients. Curr Med Res Opin 1982;8:145–9.
3. Russell AS, Aghazadeh-Habashi A, Jamali F. Active ingredient
consistency of commercially available glucosamine sulfate products. J Rheumatol
4. Houpt JB, McMillan R, Wein C, Paget-Dellio SD. Effect of glucosamine
hydrochloride in the treatment of pain of osteoarthritis of the knee. J Rheumatol
5. Tapadinhas MJ, Rivera IC, Bignamini AA. Oral glucoseamine sulfate in
the management of arthrosis: report on a multi-centre open investigation in Portugal.
6. Virkamaki A, Daniels MC, Hamalainen S, et al. Activation of the
hexosamine pathway by glucosamine in vivo induces insulin resistance in multiple insulin
sensitive tissues. Endocrinology 1997;138:2501–7.
7. Rossetti L, Hawkins M, Chen W, et al. In vivo glucosamine infusion
induces insulin resistance in normoglycemic but not in hyperglycemic conscious rats. J
Clin Invest 1995;96:132–40.
8. Barzilai N, Hawkins M, Angelov I, et al. Glucosamine-induced
inhibition of liver glucokinase impairs the ability of hyperglycemia to suppress endogenous
glucose production. Diabetes 1996;45:1329–35.
9. Russell AI, McCarty MF. Glucosamine in osteoarthritis. Lancet
1999;354:1641; discussion 1641–2 [letters].
10. Rovati LC, Annefeld M, Giacovelli G, et al. Glucosamine in
osteoarthritis. Lancet 1999;354:1640; discussion 1641–2.
11. Reginster JY, Deroisy R, Rovati L, et al. Long-term effects of
glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical
trial. Lancet 2001;357:251–6.
12. Matheu V, Bracia Bara MT, Pelta R, et al. Immediate-hypersensitivity
reaction to glucosamine sulfate. Allergy 1999;54:643–50.