The metabolic syndrome
BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7406.61 (Published 10 July 2003) Cite this as: BMJ 2003;327:61All rapid responses
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Metabolic syndrome( MetS) may be a distrating detour from EBM at
present.There is a clear need to establish the linkage between MetS and
insulin resistance (IR).There is conflicting evidence with studies showing
linkage(1)but recent studies have shown that IR is not a core component in
factor analysis of MetS (2).However,IR state does increase cardio vascular
disease(CVD) risk and the onus is on the physicians to identify IR in
every day clinical practice.It is felt that TG/HDL ratio alone could alert
the existance of IR(3).The traditional dietary approach of low fat and
high carbohydrate(CHO) diet for raised LDL levels could then make co
existing IR worse. This approach will increase
triglyceride(TG)levels.Rising TG levels are the driving force for low HDL
levels which has negative association with CVD. Clearly weight reduction
and excercise are well accepted strategies for reducing IR and CVD risk.In
addition a dietary regime of 45% CHO, 40% fat and 15% protein could be
considered appropriet if IR is present.Fat intake would be mostly in the
form of mono and poly unsaturated fat with saturated fat restricted to 7
or 8%.
References:(1) Richard P Donahue et al.Does Insulin resistance unite
the seperate components of the Insulin resistance syndrome (evidence from
Miami Community Health study)Arteriosclerosis,thrombosis and vascular
biology.1997;17:p2413-2417
(2)Ramachandran et al.Metabolic syndrome in urban asian indian adults-a
population study using modified ATP 111 criteria: Diabetes research and
clinical practice 60(2003)p199-204.
(3) Gerald Reaven MD,Metabolic syndrome Circulation.2002;106:p286-288
Competing interests:
None declared
Competing interests: No competing interests
I suggest the common link to all of this syndrome is low
dehydroepiandrosterone (DHEA).
Competing interests:
None declared
Competing interests: No competing interests
Metabolic syndrome and pregnancy induced hypertension
Pre-eclampsia, or pregnancy-induced hypertension (PIH) is a major
cause of maternal and fetal morbidity and mortality complicating 7-10% of
pregnancies (1). However, the pathogenesis of this condition remains
unclear. Many features of the insulin resistance syndrome such as
hypertension, hyperinsulinemia, glucose intolerance, obesity, and lipid
abnormalities have been associated with this condition (2). There is
increasing evidence which suggests a link between the two conditions.
It has been shown that frequencies of PIH and gestational diabetes
mellitus are increased in pregnancies in women who had poly cystic ovarian
disease, which is known to be associated with insulin resistance (3).
Although it is not clear how insulin resistance predisposes to PIH it has
been shown that insulin resistance is associated with hyperleptiaemia and
leptin resistance which is thought to result in endothelial dysfunction
(1). A higher concentration of Leptin, the obese gene product from
adipocytes, is found in normal pregnancy as it is produced by the
placenta. However, it has been shown that maternal plasma leptin levels in
severe preeclampsia are significantly higher than those in normotensive
pregnant women which could give rise to endothelial dysfunction or lead to
PIH by unknown mechanisms (4).
It is evident that the metabolic syndrome may have a role in the
pathogenesis of PIH. Therefore, women who wish to conceive should be
screened for features of metabolic syndrome such as glucose intolerance,
central obesity and lipid abnormalities with view of prevention of PIH
which results in adverse effects in both the mother and the fetus.
Reference:
1. Anderson CM, Ren J. Leptin, leptin resistance and endothelial
dysfunction in pre-eclampsia. Cell Mol Biol (Noisy-le-grand). 2002;48
Online Pub:OL323-9
2. Solomon CG, Seely EW. Brief review: hypertension in pregnancy: a
manifestation of the insulin resistance syndrome? Hypertension. 2001
Feb;37(2):232-9.
3. Bjercke S, Dale PO, Tanbo T, Storeng R, Ertzeid G, Abyholm T.
Impact of insulin resistance on pregnancy complications and outcome in
women with polycystic ovary syndrome. Gynecol Obstet Invest. 2002;54(2):94
-8.
4. Sagawa N, Yura S, Itoh H, et al. Possible role of placental leptin
in pregnancy: a review. Endocrine. 2002 Oct;19(1):65-71.
Competing interests:
None declared
Competing interests: No competing interests