The prevalence of dyslipidaemia is much more common in NIDDM as compared to IDDM. Diabetes begins with an excess of fat and diabetics die from an excess of it¹. Atherosclerosis accounts for 80% of all diabetic mortality². About 75% of atherosclerotic diabetic mortality is the consequence of coronary atherosclerosis; the remaining 25% results from a combination of accelerated cerebral vascular disease, peripheral vascular disease or both. Compared to non-diabetic patients, the incidence of CAD is twice in men with diabetes and four times in diabetic women³. Similarly, cerebral vascular and peripheral vascular diseases increased four to five fold respectively in diabetic patients compared with non-diabetic individuals². Diabetes is the most common cause of heart disease in young people⁴. Obesity, another inherent feature of NIDDM may contribute to the development of hypertriglyceridaemia and has more adverse effects on lipids and lipoproteins in NIDDM, than in IDDM⁵. The most common abnormality in diabetes is hypertriglyceridaemia, elevated very low density lipoproteins (VLDL) and decreased HDL levels⁶. NIDDM subjects have higher triglyceride levels than the general population and these levels are probably higher than in individuals with the same degree of obesity who do not have diabetes. The lower HDL cholesterol level observed in NIDDM patients is related to higher triglyceride levels, degree of central or intra-abdominal obesity, glucose and insulin levels. One of the determinants of diabetic hypertriglyceridaemia is the over-production of VLDL⁷. The abnormal lipoprotein levels characteristic of NIDDM have also been observed among "prediabetic" individuals, especially lower HDL cholesterol and higher triglyceride levels. Lipoprotein lipase depends on insulin for its full activity and VLDL clearance is reduced in poorly-controlled patients with IDDM. Low density lipoprotein (LDL) levels are also raised in association with poor glycaemic control, but a substantial improvement in blood sugar is required⁸.

Diet, exercise and glycaemic control are first-line measures for managing dyslipidaemia in the diabetic patient⁹. These measures, although often beneficial, cannot completely reverse dyslipidaemia, particularly in NIDDM patients¹⁰. Several drugs have been recommended for treating hyperlipidaemia, but they are associated with a number of side-effects.

Diabetes mellitus (Madhumeha) was known to ancient Indian physicians and an elaborated description of its clinical features and effective management appears in Ayurvedic texts. A number of herbs have been known to possess anti-diabetic properties. Diabecon (D-400), a herbomineral preparation whose main ingredients are Eugenia jambolana¹¹, Pterocarpus marsupium¹², Ficus glomerulata, Gymnema sylvestre¹³, Momordica charantia¹⁴, Ocimum sanctum¹⁵ and Shilajeet¹⁶, has been found to effectively lower the blood sugar level in NIDDM patients¹⁷. It has also been found to reduce serum cholesterol and triglyceride levels in many experimental trials¹⁸.

With the above information, a multicentric study was conducted to evaluate the efficacy of a herbomineral anti-diabetic formulation, Diabecon (D-400), on blood sugar and lipid profile in NIDDM cases.

One hundred and fifteen patients in the age range of 30-70 years who attended the OPD between Dec. 1994 and Aug. 1995 at 4 different trial centres were recruited for an open clinical trial of Diabecon (D-400). The protocol was cleared by the respective ethical committees before the commencement of the study and written informed consent was taken from all the patients before recruitment. Patients were selected on the basis of WHO criteria TRC series No. 725, 1985. A trial of diet and life-style modification alone was given to freshly diagnosed cases for a period of 3 months, failing which they were recruited for the trial. Patients with severe cardiovascular disease, pregnancy and hypertension were excluded from the trial. All the patients received Diabecon (D-400) at a dose of 2 tablets t.d.s. for a period of 6 months and lipid profile was assessed initially and after 6 months.

Statistical analysis was done by using unpaired ‘t’ test.

The initial mean serum cholesterol level was 243.60 ± 13.50mg/dl. An analysis done for 55 patients showed that the triglycerides level was 227.42 ± 22.92mg/dl and LDL was 175.40 ± 13.50mg/dl. HDL was 43.61 ± 2.07mg/dl and VLDL was 45.30 ± 4.50mg/dl.

In all patients, it was observed that there was a significant reduction in fasting and postprandial blood sugar level, with a significant decrease in total cholesterol, triglycerides, LDL and VLDL levels and a considerable increase in HDL level. At the end of 6 months, the mean total cholesterol was 188.00 ± 2.90mg/dl (p<0.01), triglycerides levels as 153.55 ± 7.70mg/dl (p<0.01), LDL was 121.00 ± 4.10mg/dl (p<0.01), VLDL was 33.50 ± 0.89mg/dl (p<0.01) and HDL was 53.34 ± 2.12mg/dl (p<0.01), which confirms the antihyperlipidaemic effect of Diabecon (D-400) (Table 1).

A sense of well-being was observed in all the patients and none of them complained of any side-effects.

Metabolic control of diabetes also improved significantly (Table 2).

Dyslipidaemia substantially increases the likelihood of serious cardiovascular problems in NIDDM patients, a population already at high risk of adverse cardiovascular changes associated with hypertension and hyperinsulinaemia.¹⁹ This constitutes an atherogenic profile and in turn may be magnified by qualitative lipoprotein changes in diabetes, such as glycosylation and oxidation.²⁰ In NIDDM patients, dyslipidaemia of this nature may be independent of glycaemic control. In the consensus statement issued by the American Diabetes Associates, it is noted that efforts to lower blood glucose are necessary but not sufficient to prevent macrovascular complications in most diabetic patients²¹. In view of the above, greater attention must be given to correct dyslipidaemia in diabetic patients who are receiving lipid lowering therapy. Although the beneficial effects of normalising lipids in NIDDM patients have not been studied in terms of reduced CAD morbidity/mortality, correction of dyslipidaemia has been shown to significantly reduce cardiac end points in non-diabetic patients with elevated plasma LDL-cholesterol, TG and low HDL-cholesterol levels⁽²²⁾.

In the present study, a significant reduction in blood lipids was observed at the end of the 6-month study period. The results of this study demonstrate that Diabecon (D-400) is effective in correcting the two most common lipid abnormalities of NIDDM, i.e. hypertriglyceridaemia and low HDL levels.

A major concern in clinical studies of this nature is the tendency for biochemical parameters to regress towards mean levels. To eliminate this possibility, a 12-week baseline period was established. Trend analysis revealed no significant changes over this period, indicating that the reduction in blood lipids represents a significant change. Body weight did not show any notable change, proving that reduction in TG and TC could be on account of subsequent reduction in both fasting and postprandial blood sugar but not due to the actual effect of the drug. Since Balsamodendron mukul, an important ingredient of Diabecon (D-400), has been proven to be effective in lowering blood lipids, it is possible that the hypolipidaemic action of Diabecon (D-400) may be independent of its usefulness in lowering blood sugar.

No primary prevention trial has so far specifically examined the effects of lipid-lowering therapy on macrovascular end points in NIDDM patients. However, improvements in the lipoprotein profiles were associated with a 34% reduction in the incidence of fatal and non-fatal coronary heart disease. What is now required is a long-term study to explore the role of Diabecon (D-400) in the progression of macrovascular disease in NIDDM.

1. Joslin EP. Arteriosclerosis and diabetes. Am. Clin. Med. 1927; (5): 1061-80.
   
   
2. Barrett-Connor E, Orchard T. Diabetes and heart disease. In: Diabetes in America: Diabetes Data Compiled 1984. Washington DC, National Diabetes Data Group. Department of Health and Human Services, 1985, 1-41 (NIH publ. no. 85-1468).
   
   
3. Kannel WB. Lipids, diabetes and coronary heart disease: insights from the Framingham study. Am. Heart J. 1985; 110: 1100-107.
   
   
4. American Diabetes Association: Consensus statement: role of cardiovascular risk factors in prevention and treatment of microvascular disease in diabetes. Diabetes Care 1989; 12: 573-9.
   
   
5. Laakso M, Pyorala K, Adverse effects of obesity on lipid and lipoprotein levels in insulin dependent and non-insulin-dependent diabetes. Metabolism 1988; 39: 117.
   
   
6. Albrink MJ. Dietary and drug treatment of hyperlipidaemia in diabetes. Diabetes 1974; 23: 913.
   
   
7. Kissebah AH, Alfarsi S, Evans DJ, Adams PW. Integrated regulation of very low density lipoprotein triglyceride and apolipoprotein-B kinetics in non-insulin-dependent diabetes mellitus. Diabetes 1987; 31: 903.
   
   
8. Pietri A, Dunn FL, Raskin P. The effect of improved diabetic control on plasma lipid and lipoprotein levels. A comparison of conventional therapy and continuous subcutaneous insulin. Diabetes 1980; 29: 1001.
   
   
9. American Diabetes Association: Consensus statement. Role of cardiovascular risk factors in prevention and treatment of microvascular disease in diabetes. Diabetes Care 1989; 12: 573-9.
   
   
10. Brunzell JD, Hazzard WR, Murulsky AG, Bierman EL. Evidence for diabetes mellitus and generic forms of hypertriglyceridaemia as independent entities. Metabolism 1975; 24: 1115-21.
    
    
11. Hollenbeck CB, Chen YD, Greenfield MS, Lardinois CK, Reaven GM. Reduced plasma high density lipoprotein-cholesterol concentrations need not increase when hyperglycaemia is controlled with insulin in non-insulin-dependent diabetes mellitus. J. Clin. Endocrinol. Metab 1985; 65: 605-8.
    
    
12. Jose MP et al. Effects of selected indigenous drugs on blood sugar levels in dogs. Ind. J. Pharmacol 1976; 86.
    
    
13. Gupta SS, Variyurm MC. Inhibitory effect of Gymnema sylvestre (Gurmar) of adrenohypophyseal activity in rats.
    
    
14. Kedar P, Chakrabarti CH. Effect of bitter gourd seeds and glibenclamide in streptozotocin-induced diabetes mellitus. Ind. J. Exp. Biol. 1982; 20: 232.
    
    
15. Chhatopadhyay R. Hypoglycaemic effect of Ocimum sanctum leaf extract in normal and streptozotocin-induced diabetes mellitus. Ind. J. Exp. biol. 1982; 20: 232.
    
    
16. Gupta SS, Sethi CB, Mathur VS. Effect of Gurmar and Shilajeet on body weight of young rats, Ind. J. Physiol. Pharmacol 1976; 9: 22, 87.
    
    
17. Ganguly D, Banerjee T, Singh AK, Mitra SK. Effect of D-400, an Ayurvedic herbomineral formulation in non-insulin-dependent diabetes mellitus cases. The Antiseptic 1995; 92: 12, 460-2.
    
    
18. Mitra SK, Gopumadhavan S, Muralidhar TS, Anturlikar SD, Sujatha MB. Effect of Diabecon (D-400), a herbomineral preparation on lipid profile, glycated haemoglobin and glucose tolerance in streptozotocin-induced diabetes in rats. Ind. J. Exp. Biol. 1995; 33: 10, 798.
    
    
19. Hamilton BP. Diabetes mellitus and hypertension. Am. J. Kidney Dis 1990; 16: 20.
    
    
20. Austin MA, King MC, Vramzan KM, Krauss RM. Atherogenic lipoprotein phenotype: a proposed genetic marker for coronary heart disease risk. Circulation 1990; 82: 495.
    
    
21. Ho LT, Li SH, Show TY, Liu YF, Perng JC, Hau HK, Chen JJ. Gemfibrozil has antilipidaemic effects on diabetic patients with hyperlipidaemia. Clin. Med. J. 1986; 39: 1.
    
    
22. Frick MH, Elo O, Haapa K, Heimonen OP, Haimsalim P, Helo P, Nikkila EA, Helsinki Heart study: primary prevention trial with gemfibrozil in middle-aged men with dyslipidaemia. N. Engl. J. Med. 317: 1237.