J. Lipid Res. Please sign the JLR Guestbook
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Aguilar-Salinas, C. A.
Right arrow Articles by Sepulveda, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Aguilar-Salinas, C. A.
Right arrow Articles by Sepulveda, J.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Journal of Lipid Research, Vol. 42, 1298-1307, August 2001
Copyright © 2001 by Lipid Research, Inc.

Original Article

High prevalence of low HDL cholesterol concentrations and mixed hyperlipidemia in a Mexican nationwide survey

Carlos A. Aguilar-Salinasa, Gustavo Olaizb, Victoria Vallesa, Juan Manuel Ríos Torresa, Francisco J. Gómez Péreza, Juan A. Rulla, Rosalba Rojasb, Aurora Francob, and Jaime Sepulvedab
a Departamento de Endocrinología y Metabolismo de Lípidos, del Instituto Nacional de Ciencias Médicas y Nutrición, Vasco de Quiroga 15, Mexico City 14000, Mexico
b Instituto Nacional de Salud Publica, Cuernavaca, Morelos, Mexico

Correspondence to: Carlos A. Aguilar-Salinas, To whom correspondence should be addressed., caguilarsalinas{at}yahoo.com (E-mail)


  ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES

The prevalence of lipid abnormalities revealed in a survey done in 417 Mexican cities is described. Information was obtained on 15,607 subjects, aged 20 to 69 years. In this report, only samples obtained after a 9- to 12-h fast were included (2,256 cases: 953 men and 1,303 women). The population is representative of Mexican urban adults. Mean lipid concentrations were: cholesterol, 4.80 mmol/l; triglycerides, 2.39 mmol/l; HDL cholesterol, 1.00 mmol/l; and LDL cholesterol, 3.06 mmol/l. The most prevalent abnormality was HDL cholesterol below 0.9 mmol/l (46.2% for men and 28.7% for women). Hypertriglyceridemia (>2.26 mmol/l) was the second most prevalent abnormality (24.3%). Severe hypertriglyceridemia (>11.2 mmol/l) was observed in 0.42% of the population. Increased LDL cholesterol (>=4.21 mmol/l) was observed in 11.2% of the sample. Half of the hypertriglyceridemic subjects had a mixed dyslipidemia or low HDL cholesterol. More than 50% of the low HDL cholesterol cases were not related to hypertriglyceridemia. Insulin resistance was found in 59% of them.

In conclusion, the prevalence of hypoalphalipoproteinemia and other forms of dyslipidemia in Mexican adults is very high and it is among the highest previously reported worldwide. — Aguilar-Salinas, C. A., G. Olaiz, V. Valles, J. M. Ríos Torres, F. J. Gómez Pérez, J. A. Rull, R. Rojas, A. Franco, and J. Sepulveda. High prevalence of low HDL cholesterol concentrations and mixed hyperlipidemia in a Mexican nationwide survey. J. Lipid Res. 2001. 42: 1298;–1307.

Supplementary key words: diabetes, obesity, hypertension, cholesterol, Mexico, insulin resistance, hypertriglyceridemia


  INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES

The chronic-degenerative disorders have become a growing health problem in Mexico. Coronary heart disease and diabetes are the first and fourth leading causes of death in Mexico, followed by stroke as the fifth leading cause (1). The interaction between genetic and environmental factors explains the increasing magnitude of the phenomenon. Several authors have demonstrated that the Mexican population has a genetic predisposition to the metabolic syndrome type 2 diabetes and several primary forms of dyslipidemias (2) (3) (4). A high-fat, high-carbohydrate, calories-rich diet; tobacco use; alcohol consumption; and the sedentary lifestyle of a large proportion of the population are among the recognized environmental factors (5) (6) (7).

During the past decade, a vast amount of evidence has confirmed the critical role played by the dyslipidemias in the pathogenesis of atherosclerosis (8) (9) (10) (11) (12). Multiple studies have shown that modification of the plasma lipid concentrations is a useful approach in decreasing cardiovascular mortality (13) (14) (15). Several studies have demonstrated that the prevalence of some forms of the dyslipidemias is high in Mexico (16); the 1988 National Seroe-pidemiologic Survey showed that the prevalence of hypercholesterolemia found in northern Mexico is similar to that reported in the United States (17). Smaller studies also have suggested that hypertriglyceridemia and hypoalphalipoproteinemia are frequent risk factors in Mexican adults (18) (19). On the basis of the age distribution of the Mexican population, composed mainly of those 30 years old and younger, it is very likely that the prevalence of the lipid abnormalities will be even greater in the next few decades. Periodic studies of the prevalence of the main coronary risk factors will help to predict the trends on cardiovascular mortality for upcoming years and will help in designing preventive strategies to cope with this health problem.

In the period 1992;–1993, the Ministry of Health of Mexico conducted the National Survey of Chronic Diseases to estimate the prevalence of obesity, type 2 diabetes, renal pathology, hypertension, and dyslipidemia. The objective of this article is to describe the prevalence, by age and gender, of the lipid abnormalities revealed in the survey. The results are presented using an epidemiological and a clinically oriented approach.


  MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES

Population sample
This is a cross-sectional study that includes individuals from cities with more than 2,500 people. A multistage sampling procedure was used. The country was divided into four regions: northern, central, and southern, composed of 10 states each, and the metropolitan area of Mexico City (including the remaining two states). A random sample of Basic Geographical Statistical Units was obtained in each state from a database recently generated by the Instituto Nacional de Geografía y Estadística and after the general sampling frame was constructed by the Health Ministry. Neighborhood blocks were randomly selected and all adults (aged 20 to 69 years) in all households of the selected blocks were surveyed (with the exception of those living in military, religious, and health and other institutions). A total of 417 cities were studied. The sample was representative of the Mexican urban population, which in 1990 constituted 71% of the total population (20). A target of 4,731 individuals and 2,030 households per region was estimated using the household as the sampling unit and using the average of 2.33 adults per household (according to the 1990 National Census). The sample size was considered sufficient to detect risk factors at the regional level, that have at least a prevalence of 4% with a relative error of estimation of 0.289 and a nonresponse rate of 30%. Information was obtained on 15,607 individuals; the response rate was 82.5%. The study was conducted in accordance with the Helsinki Declaration of Human Studies.

Personal interview
A general structured interview was conducted. A previously standardized questionnaire was used to obtain information on demographic and socioeconomic aspects, family health history, personal medical history, and lifestyle factors, such as smoking. In the same visit, anthropometric and blood pressure measurements were obtained. Systolic (1st-phase) and diastolic (5th-phase) blood pressures were measured to the nearest even digit with a sphygmomanometer while the subject was in the supine position after a 5-min rest. Participants removed their shoes and upper garments. Height was measured to the nearest 0.5 cm. Body weight was measured on a daily calibrated balance and recorded to the nearest 0.1 kg. Body mass index (BMI) was calculated as weight (kg), divided by height (m2), and was used as an index of overall adiposity. The equipment was regularly calibrated using reference samples provided by the manufacturer.

Methods
Blood samples were obtained from 77.6% of the population (n = 14,682). This report includes the results from 2,256 subjects who had a 9- to 12-h fasting period, required for a complete lipid profile (15.3% of the population). These cases were randomly distributed among the population; no bias was detected for regional or socioeconomic status in this subset of cases. All analytical measurements were done at the Departamento de Endocrinología and Metabolismo of the Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán." The sampling procedure was standardized during a 28-week training course. The subjects were sampled at their homes; they remained seated for 5 min before blood was drawn.

Plasma glucose was analyzed by the glucose-oxidase method (Boehringer-Mannheim). Plasma concentrations of total cholesterol and triglycerides were determined by enzymatic methods (Boehringer-Mannheim). HDL cholesterol was measured after precipitation of VLDL and LDL by the phosphotungstate method (Boehringer-Mannheim); LDL cholesterol was measured by beta quantification. Intra-assay CV values for total cholesterol, triglycerides, and HDL cholesterol were 3%, 5%, and 5%, respectively. Insulin was analyzed by ELISA in the ES-33 system (Boehringer-Mannheim). The cross-reactivity with proinsulin for this assay was 40%. Our laboratory followed standardization procedures according to the recommendation of the World Health Organization, including the use of external control sera.

Definitions
Three different cutpoints were used to analyze the prevalence of hypertriglyceridemia, based on the different existing consensus recommendations. The selected cutpoints were 1.58, 2, and >=2.2 mmol/l (21) (22) (23). A cholesterol >=6.3 mmol/l was considered to be hypercholesterolemia. HDL cholesterol concentration was considered to be abnormal if it was <0.9 mmol/l. Mixed hyperlipidemia was defined as cholesterol >=5.2 mmol/l plus triglycerides >=2.26 mmol/l. Severe hyperlipidemia was defined as cholesterol >=7.8 mmol/l and/or triglycerides >=5.6 mmol/l. Normotriglyceridemic hypoalphalipoproteinemia was defined as HDL cholesterol <0.9 mmol/l and triglycerides <2.26 mmol/l. Isolated hypertriglyceridemia was defined as an increased triglyceride concentration and a cholesterol <5.2 mmol/l. These cutpoints were based on the 1992 recommendations of the European Atherosclerosis Society (24). Overweight was defined as BMI 25;–30 kg/m2 for males and females. Obesity was defined as BMI >=30 kg/m2. Individuals were diagnosed as diabetics if they had a previous diagnosis of diabetes or had a fasting blood glucose value >=7 mmol/l (126 mg/dl) and no previous history of diabetes. Hypertension was diagnosed when the subject's systolic pressure was >=140 mm Hg and/or diastolic pressure was >=90 mm Hg and/or the subject currently used an antihypertensive medication. Blood pressure was measured twice in two different visits if the initial measurement was >=120/80. Ischemic heart disease was considered if there was a history of myocardial infarction. Homeostasis model (HOMA) scores were used for assessing insulin sensitivity. Subjects with a value above 2.4 were considered insulin resistant. This cutpoint represents the 90th percentile of the general population in this survey; similar cutpoints had been used in previous reports (25).

Statistical analysis
The data were codified and captured under ASCII fixed format. The database was validated through recognition of missing values, outliers, and inconsistencies among variables. Descriptive analysis included the estimation of mean values and standard deviations for continuous variables. These values were rounded to the nearest integer or first decimal. Prevalence and frequencies are expressed in term of percentage. The ANOVA test was applied to compare differences among the subgroups of the population. Categorical variables were compared by the chi square statistic with Yates' Correction for Continuity or the Fisher Exact Test when appropriate. All the statistical analysis was conducted in SPSS for Windows.


  RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES

The study included 2,256 subjects (953 men and 1,303 women). Most subjects were younger than 40 years old; the age distribution is representative of Mexican adults ( Table 1 and Table 2). Mean lipid concentrations were cholesterol, 4.8 mmol/l (182.7 mg/dl); triglycerides, 2.3 mmol/l (213.4 mg/dl); HDL cholesterol, 1.0 mmol/l (38.3 mg/dl); and LDL cholesterol, 3.0 mmol/l (116.4 mg/dl). The distribution by percentiles, stratified by age and gender, of the cholesterol, triglycerides, LDL cholesterol, and HDL cholesterol concentrations is shown in Table 1.


 
View this table:
[in this window]
[in a new window]
  		Table 1. Distribution of cholesterol, triglycerides, HDL, and LDL cholesterol concentrations in urban Mexican adults


 
View this table:
[in this window]
[in a new window]
  		Table 2. Prevalence of lipid abnormalities in men, women, and both genders in general population

Prevalence of isolated lipid abnormalities
The prevalence of hypertriglyceridemia, hypercholesterolemia, and hypoalphalipoproteinemia is shown in Table 2. The data are stratified by age and gender. The most common abnormality was a low HDL cholesterol concentration (46.2% for men, 28.7% for women, and 36% for both genders). The second most common abnormality was hypertriglyceridemia. Several cutpoints, based on the current available consensus, were used. Even with the less strict criteria, more than 10% of the subjects aged 20 to 29 years had this abnormality; this defect was more frequent in men. Severe hypertriglyceridemia [>11.2 mmol/l (1000 mg/dl)] was found in 0.5% of men, 0.16% of women, and in 0.4% of both genders. Increased LDL cholesterol concentrations (>=160 mg/dl) were observed in 12.7% of men, 10.3% of women, and 11.2% of both genders. As expected, the prevalence of hypercholesterolemia was higher in older individuals and in men.

Prevalence of lipid phenotypes
The lipid abnormalities could be due to multiple etiologies and are associated with different cardiovascular risk factors. This statement is especially true for hypertriglyceridemia. Thus, the crude description of the prevalence of the isolated lipid abnormalities is a gross estimation of the lipid related cardiovascular risk of a population. A more precise description is obtained when the lipid abnormalities are grouped as lipid phenotypes. The prevalence of the most relevant lipid phenotypes is shown in Table 3 Table 4 Table 5 Table 6 Table 7.


 
View this table:
[in this window]
[in a new window]
  		Table 3. Prevalence of several abnormal lipid patterns in men, women, and both genders in general population


 
View this table:
[in this window]
[in a new window]
  		Table 4. Prevalence of several abnormal lipid patterns in men, women, and both genders in general population


 
View this table:
[in this window]
[in a new window]
  		Table 5. Prevalence of several abnormal lipid patterns in both genders with type 2 diabetes (n = 193)


 
View this table:
[in this window]
[in a new window]
  		Table 6. Prevalence of several abnormal lipid patterns in obese (n = 452) and overweight (n = 787) subjects


 
View this table:
[in this window]
[in a new window]
  		Table 7. Prevalence of several abnormal lipid patterns in both genders with hypertension (n = 492)

Hypertriglyceridemia/hypoalphalipoproteinemia
This atherogenic profile, usually seen in the insulin resistance syndrome, was observed in 12.9% of the general population (Table 3). The prevalence was significantly higher in men compared with women (20.9% vs. 7.2%, respectively, P < 0.01). In men, the prevalence at ages 20 to 29 was almost as high as that observed in women ages 50 to 59 (13.1% vs. 15%, respectively). After age 60, its prevalence decreased, suggesting a survival effect.

Normotriglyceridemic hypoalphalipoproteinemia
This profile was among the most common forms of dyslipidemias in the population reported here (18.6% of general population). The prevalence was higher in men than in women (22% vs. 16%, respectively, P < 0.05). The prevalence found in young men (23.1%) was similar to that observed in men aged 50 to 59 (26.5%). A survival effect was found in women older than 50 years (Table 4). Several etiologies may be present in this group. Tobacco was used by 31.2% of these subjects. Insulin resistance, assessed by a HOMA value above 2.4, was found in 59% of this group. Thirty-six percent had a BMI between 25 and 30 kg/m2, and 20.9% had a value higher than 30 kg/m2. Less than 1% had a BMI lower than 18 kg/m2.

Mixed hyperlipidemias
The simultaneous elevation of cholesterol and triglyceride concentrations was observed in 12.6% of the general population (Table 3). Close to 20% of subjects over 50 years old had a mixed dyslipidemia. This abnormality was more frequent in men than in women (16.8% vs. 9.6%, respectively, P < 0.01), especially at ages 50 to 59. This defect was also common in young men (8.1%).

Severe dyslipidemias
Extreme elevations of triglycerides (5.6 mmol/l or 500 mg/dl) were the most common form of severe dyslipidemia (Table 3). This abnormality was observed in 2.9% of the general population. On the other hand, extreme cholesterol elevations (>7.8 mmol/l or 300 mg/dl) with normal triglycerides levels were found in only 0.29% of the cases. The prevalence of severe hypertriglyceridemia was higher in men than in women (5.5% vs. 1.4%, respectively). Remarkably, 3.1% of men aged 20 to 29 years had this defect.

Isolated hypertriglyceridemia
Small differences in the diagnostic criteria had a large impact on the prevalence of this abnormality (Table 4). A 0.5 mmol/l (50 mg/dl) difference (from 1.6 to 2.2 mmol/l) resulted in a 100% increase in the prevalence, from 15.8% to 31.8%. Even by using the least strict criteria, the prevalence of this lipid profile was high, ranging from 10.2% in the youngest subjects to 26% in the oldest group. This abnormality was more common in men than in women (21.3% vs. 12.1%, respectively). More than 30% of men older than 50 years old had a fasting triglyceride concentration above 2.2 mmol/l (200 mg/dl).

Isolated hypercholesterolemia
Cases with increased cholesterol concentration and triglycerides below 2.2 mmol/l were included in this category (Table 4). Isolated hypercholesterolemia was found in 18.7% of the population. The vast majority of cases had a cholesterol concentration between 5.2 and 6.3 mmol/l (200 and 240 mg/dl); only 3.5% of all individuals had concentrations above this range. Close to 10% of the youngest group had cholesterol between 5.2 and 6.3 mmol/l (200 and 240 mg/dl); women above age 50 composed the group in which this abnormality was most common (~41%).

Effects of diabetes on the prevalence of lipid abnormalities
One hundred ninety-three patients with diabetes were included. Due to the sample size, the results were stratified only by age. As shown in Table 5, isolated hypertriglyceridemia (54.9%), isolated hypercholesterolemia (42.5%), and mixed dyslipidemias (31%) were the most prevalent abnormal lipid profiles in the patient with diabetes. This disorder increased the likelihood of having almost every class of lipid abnormality. The risk was statistically significant for mixed dyslipidemias (OR 3.1), severe dyslipidemias (OR 4.7), isolated hypertriglyceridemia (OR 6.4), and isolated hypercholesterolemia (OR 5.7). The combination hypertriglyceridemia/hypoalphalipoproteinemia was found in 26% of the diabetic population. Severe hypertriglyceridemia was found in 10.8%. Normotriglyceridemic hypoalphalipoproteinemia was found in 7.6% of cases.

Effects of overweight and obesity on the prevalence of lipid abnormalities
Four hundred fifty-two obese individuals (BMI >30 kg/m2) and 787 overweight individuals (BMI 25;–30 kg/m2) were included in the analysis. Due to the sample size, the results were stratified only by age. As shown in Table 6, the prevalence of abnormal lipid profiles was very similar between obese and overweight subjects. Hypertriglyceridemia (35.4% and 32.5%, respectively) and mixed dyslipidemias (18% and 18.1%, respectively) were the most prevalent abnormal lipid profiles in these subjects. Obesity increased the prevalence of almost every abnormal lipid profile; however, none of the odds ratios were statistically significant. The combination hypertriglyceridemia/hypoalphalipoproteinemia was found in nearly 20% of the subjects. Severe hypertriglyceridemia was found in a percent similar to that observed in the general population. Decreased HDL cholesterol, not related to hypertriglyceridemia, was found in 19% of cases.

Effects of hypertension on the prevalence of lipid abnormalities
Four hundred ninety-two hypertensive subjects were included in the analysis. As shown in Table 7, the prevalence of the abnormal lipid profiles was higher in the hypertensive subjects compared with the general population; however, none of the odds ratios was statistically significant. Hypertriglyceridemia (36.5%) and mixed dyslipidemias (21.2%) were the abnormalities most frequently observed in this subset of the population.


  DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES

These data clearly demonstrate that some forms of dyslipidemias are very common in Mexican adults. Close to 50% had hypoalphalipoproteinemia (<0.9 mmol/l, 35 mg/dl) and almost a third of the population had fasting triglycerides above 2.26 mmol (200 mg/dl). In some subsets of the population the problem was even worse. Prevalence was higher in men, especially when they were older than age 50. Hypercholesterolemia was significantly less common compared with the two aforementioned abnormalities. Moreover, the majority of these subjects had cholesterol concentrations between 5.2 and 6.3 mmol/l (200;–240 mg/dl); only 10% of the population had a cholesterol level high enough to consider the subject at risk due only by its presence.

Dyslipidemias are caused by the interaction of genetic and environmental factors. As shown in Table 8, the prevalence of the lipid abnormalities reported here is similar to that observed in Turkish (26) and other Asian populations, including Bangladeshi and Pakistani populations (27). Like Mexican adults, Turks have a high incidence of coronary heart disease (estimated by the Turkish Ministry of Health to cause 37% of deaths), although the mean cholesterol and LDL cholesterol concentrations are remarkably lower compared with ethnic groups with high rates of cardiovascular mortality. These populations have one of the highest prevalences of low HDL cholesterol worldwide (53% of males and 26% of women). Genetic factors seem to be part of the explanation of this abnormality, since HDL cholesterol levels remain low in Turks living in different environments. Mexican American women had significantly lower HDL cholesterol levels than did white US females in the NHANES III report (1.39% vs. 1.47% mmol/l, respectively). These observations suggest that the genetic factors causing low HDL cholesterol levels may be common to both ethnic groups. Genetic similarities between Mexican and Turkish populations have been described in other disorders, such as Behcet's Syndrome [based on the high frequency of HLA-B5 found in both populations (28)]. Recently, increased hepatic lipase activity has been described as a possible cause of low HDL cholesterol in Turkish men (29). This abnormality remains to be studied in our population.


 
View this table:
[in this window]
[in a new window]
  		Table 8. Comparison of serum lipid levels among Mexican, Mexican American, Turkish, and several other populations

One approach to analyzing the influence of environmental factors is to assess the prevalence of dyslipidemias in subjects with similar genetic backgrounds living in different environments. Compared with Mexican Americans, Mexican adults had significantly lower HDL cholesterol concentrations (18). These observations suggest that environmental factors may also be part of the explanation for the high frequency of hypoalphalipoproteinemia observed in Mexico. Remarkable differences exist between Mexican and Mexican American adults regarding nutrient intakes. The proportion of calories obtained from carbohydrates is significantly higher in Mexicans than in Mexican Americans (51.6% vs. 45.8%, respectively) (30). Even English-speaking Mexican American women eat greater amounts of fat (mainly saturated fat) and lower amounts carbohydrates and fiber than Mexican American women born in Mexico (31). The high consumption of simple carbohydrates may contribute to the high prevalence of hypertrigliceridemia and low HDL cholesterol (32). Also, high consumption of saturated fats raises apoA-I concentration (and HDL cholesterol) by increasing production rate and decreasing fractional catabolic rate without altering apoA-I mRNA levels (33). However, if hypertriglyceridemia results from the change in the dietary habits, the increase of HDL cholesterol may be blunted. These data suggest dietary factors contribute to the high prevalence of hypoalphalipoproteinemia and hypertriglyceridemia revealed in this report.

We propose that the very high prevalence of low HDL cholesterol in urban Mexican adults results from two groups of abnormalities. Low HDL cholesterol is explained in close to 50% of the cases by the coexistence of hypertriglyceridemia. An inverse relationship exists between fasting triglycerides and HDL cholesterol concentrations. In these cases, HDL cholesterol is normalized as triglycerides return to normal. The other 50% of cases (isolated low HDL cholesterol) may result from the coexistence of insulin resistance (34), malnutrition, low-fat content diet (35), tobacco use, and/or genetic factors to be identified. Not every one of these mechanisms is associated with an increased cardiovascular risk. However, in this population, insulin resistance, excess body fat, and/or tobacco use seems to be present in close to 60% of the subjects.

The distribution of the lipid concentrations reported here is remarkably different from that of Mexican Americans living in the US. Almost every percentile value of the cholesterol distribution is 0.5 mmol/l (~20 mg/dl) lower in the population reported here. Prevalence of hypercholesterolemia (>=6.3 mmol/l, 240 mg/dl) in Mexican adults was lower than that observed in Mexican Americans in the NHANES II and III reports (10% vs. 16.6% and 16.9%, respectively); Mexican Americans had the lowest prevalence of hypercholesterolemia of the race groups included in those reports (36). Hypercholesterolemia was twice as frequent in US white males compared with Mexican males included in this study. These observations suggest that genetic factors may protect the Mexican population against hypercholesterolemia, but, still, environmental factors, such as the growing consumption of dietary cholesterol and saturated fat, could increase the prevalence of hypercholesterolemia in urban Mexico in the near future. As the environmental conditions of urban Mexicans get closer to the prevailing conditions confronted by Mexican Americans, the prevalence of hypercholesterolemia may increase.

Our data are in accordance with previous reports in Mexican populations (17) (19) (37) (38). The prevalence of hypercholesterolemia (>=6.3 mmol/l, 240 mg/dl) reported here was almost identical to that reported in the 1988 National Seroepidemiologic Survey (10% vs. 10.6%, respectively), composed of 33,558 samples randomly obtained in adults older than 20 years (17). Unfortunately, triglycerides and HDL cholesterol concentrations were not included in that survey. In contrast to other reports, we present the results not only showing the prevalence of isolated lipid abnormalities. We believe that a more clinically oriented approach, the classification by lipid phenotypes, gives a better picture of the lipid-related atherogenic risk of the population. This is especially true for the study of hypertriglyceridemia, an abnormality caused by either atherogenic or nonatherogenic disorders (39) (40). This approach has been successfully used in the PROCAM study, a prospective study done with 4,559 men in Germany (41). This study shows that the cardiovascular risk of hypertriglyceridemic subjects is strongly influenced by the concurrent cholesterol and HDL cholesterol levels. Whereas the cardiovascular event rate of the subjects with high triglycerides and normal cholesterol (<5.2 mmol/l) was the same as that of normolipidemic controls, the risk was at least two times higher in cases with mixed dyslipidemia. This observation has important implications to our results. Of the 30% of subjects with a triglyceride level above 2.2 mmol, only half of them have a mixed dyslipidemia or low HDL cholesterol. Consequently, the crude analysis of the high prevalence hypertriglyceridemia will overestimate the cardiovascular risk of our population. This approach has two additional advantages. First, it allows also to discriminate that hypercholesterolemia was explained by the plasma accumulation of LDL in three of every four cases; in close to 25%, the correct diagnosis was a mixed dyslipidemia instead of isolated hypercholesterolemia. Second, as previously described, it shows that close to 50% of the low HDL cholesterol cases are not related to a fasting triglyceride concentration above 2.2 mmol/l. In both instances, this differentiation is important on the basis of its diagnostic and therapeutic implications (42) (43).

The prevalence of some of the lipid profiles deserves additional comments. First, almost every abnormal lipid profile was more common in males. Second, using the results of the PROCAM study as a reference (44), some major differences were found in our population. The prevalence of mixed dyslipidemias is remarkably higher in this report, especially in women. In the PROCAM study, the prevalence observed in 50-year-old men and women was 16.1% and 3.8%, respectively. As shown in Table 3, in our population, at age 50, 27.6% of men and 21.2% of women had this abnormal lipid profile. These data suggest that the most common causes of mixed dyslipidemias, such as type 2 diabetes and familial combined hyperlipidemia (44) (45), are common abnormalities in Mexico (46). Another major difference is found in the prevalence of severe dyslipidemias. In that report, the most common form of severe dyslipidemia was cholesterol above 7.8 mmol (300 mg/dl). In contrast, in our population, severe hypertriglyceridemia was several times more common than severe hypercholesterolemia. Almost 3% of the adults had triglyceride levels that could put them at risk of having acute pancreatitis. These data suggest that some actions (including decreasing consumption of simple carbohydrates and alcohol) are required in a large number of Mexican adults to prevent a rising prevalence of pancreatitis (47). Finally, the prevalence of some of the atherogenic lipid profiles shown in Table 3 was remarkably high in the younger subjects. Close to 7% had hypertriglyceridemia/hypoalphalipoproteinemia, 10% had hypercholesterolemia, and 20% had isolated low HDL cholesterol levels. These data suggest that as these individuals get older, the prevalence of atherogenic lipid profiles will be even greater. Taken together these observations suggest that the prevalence of the atherogenic lipid profiles is different in Mexican adults compared with Caucasian populations. The data reported here clearly demonstrate that effective preventive programs are urgently needed in Mexico, especially for young males.

Finally, the impact of diabetes, obesity, and arterial hypertension on the prevalence of several lipid abnormalities was assessed. As expected, these disorders were associated with an increased likelihood of having several forms of atherogenic lipid profiles (48). The most common abnormalities found in patients with type 2 diabetes were isolated hypertriglyceridemia, followed by moderated hypercholesterolemia and mixed hyperlipidemia. The same trend was observed for obesity and arterial hypertension, but the magnitude of the risk was lower with these two factors. Interestingly, the prevalence of lipid abnormalities was similar in overweight subjects compared with obese individuals, suggesting that the lipid comorbidities appear early in the development of excessive fat accumulation.

In conclusion, our data show that the prevalence of hypoalphalipoproteinemia and other forms of dyslipidemia is very high in Mexican adults and it is among the highest previously reported worldwide. Genetic and environmental factors may contribute to the explanation of the high prevalence reported here. Preventive programs are urgently needed in Mexico for decreasing the prevalence of several forms of dyslipidemia. We believe that these programs must consider decreasing the prevalence of obesity as the main goal (49). A huge educational effort geared toward the general population and physicians will be required. However, it would be worst to wait and treat millions of subjects, many of them, young and at the top of their productivity.


  FOOTNOTES

Abbreviations: apoA-I, apolioprotein A-I; BMI, body mass index; HOMA, homeostasis model. Back


  ACKNOWLEDGMENTS

The authors thank Gustav Schonfeld for thoughtful review of the manuscript.

Manuscript received January 5, 2001; and in revised form March 20, 2001


  REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES

  1. de Salud, S. 1999. Dirección General de Epidemiologia. Mexico.

  2. Stern, M. P., Knapp, J. A., Hazuda, H. P., Haffner, S. M., Patterson, J. K., Mitchell, B. D. 1991. Genetic and environmental determinants of type II diabetes in Mexican Americans. Is there a "descending limb" to the modernization/diabetes relationship? Diabetes Care. 14:649-654[Abstract].

  3. Arroyo, P., Loria, A., Fernandez, V., Flegal, K. M., Kuri-Morales, P., Olaiz, G., Tapia-Conyer, R. 1991. Obesity in Hispanic Americans. Diabetes Care. 14:691-694[Abstract].

  4. Gonzalez, C., Stern, M. P., Gonzalez, E., Rivera, D., Simon, J., Islas, S., Haffner, S. 1999. The Mexico City Diabetes Study: a population-based approach to the study of genetic and environmental interactions in the pathogenesis of obesity and diabetes. Nutr. Rev. 57:S71-S76[Medline].

  5. Hill, J. O. 1998. Genetic and environmental contributions to obesity. Am. J. Clin. Nutr. 68:991-992[Medline].

  6. Esparza, J., Fox, C., Harper, I. T., Bennett, P. H., Schulz, L. O., Valencia, M. E., Ravussin, E. 2000. Daily energy expenditure in Mexican and USA Pima Indians: low physical activity as a possible cause of obesity. Int. J. Obes. Relat. Metab. Disord. 24:55-59[Medline].

  7. Munoz de Chavez, M., Chavez-Villasana, A., Chavez-Muñoz, M., Eichin-Vuskovic, I. 2000. Sale of street food in Latin America. The Mexican case: joy or jeopardy? World Rev. Nutr. Diet. 86:138-154[Medline].

  8. Stamler, J., Wentworth, D., Neaton, J. 1986. Is the relationship between serum cholesterol and risk of death from coronary heart disease continuous and graded? Findings on the 356,222 primary screens of the Multiple Risk Factor Intervention Trial (MRFIT). J. Am. Med. Assoc. 25:2823-2829.

  9. Rose, G., Shipley, M. 1986. Plasma cholesterol and death from coronary disease: 10 year results of the Whitehall study. Br. Med. J. 29:306.

  10. Gotto, A. M. 1998. Risk factor modification: rationale for management of dyslipidemia. Am. J. Med. 104:6S-8S[Medline].

  11. Castelli, W. P. 1984. Epidemiology of coronary heart disease. The Framingham Study. Am. J. Med. 7:4.

  12. Grundy, S. M., Pasternak, R., Greenland, P., Smith, S., Fuster, V. 1999. Assessment of cardiovascular risk by use of multiple risk factor assessment equations. Circulation. 100:1481-1492[Free Full Text].

  13. Fager, G., Wiklung, O. 1997. Cholesterol reduction and clinical benefit. Are there limits to our expectations? Arterioscler. Thromb. Vasc. Biol. 17:3527-3533[Abstract/Free Full Text].

  14. Miettinen, T., Pyöralä, K., Olsson, A., Musliner, T., Cook, T., Faergeman, O., Berg, K., Pedersen, T., J. Kjelshus for the Scandinavian Simvastatin Study Group,. 1997. Cholesterol lowering therapy in women and elderly patients with myocardial infarction or angina pectoris. Circulation. 96:4211-4218[Abstract/Free Full Text].

  15. Shepherd, J., Cobbe, S. M., Ford, I., Isles, C. G., Lorimer, A. R., MacFarlane, P. W., McKillop, J. H., Packard, C. J. 1995. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N. Engl. J. Med. 333:1301[Abstract/Free Full Text].

  16. Quibrera, I. R., Hernández, H. G., Aradillas, C. G. 1994. Prevalencia de diabetes, intolerancia a la glucosa, hiperlipidemia y factores de riesgo en función de nivel socioeconómico. Rev. Invest. Clin. 44:321-328.

  17. Posadas-Romero, C., Tapia-Conyer, R., Lerman-Garber, I., Zamora-González, J., Cardoso-Saldaña, G., Salvatierra-Izaba, B., Sepúlveda-Amor, J. 1995. Cholesterol levels and prevalence of hypercholesterolemia in a Mexican adult population. Atherosclerosis. 118:275-284[Medline].

  18. Stern, M. P., Gonzalez-Villalpando, C., Mitchell, B., Villalpando, E., Haffner, S., Hazuda, H. 1992. Genetic and environmental determinants of type II diabetes in Mexico City and San Antonio. Diabetes. 41:484-492[Abstract].

  19. Fanghanel-Salmon, G., Sanchez-Reyes, L., Arellano-Montaño, S., Valdes-Liaz, E., Chavira-Lopez, J., Rascon-Pacheco, R. A. 1997. The prevalence of risk factors for coronary disease in workers of the Hospital General de Mexico. Salud. Publica. Mex. 39:427-432[Medline].

  20. Instituto Nacional de Geografia y Estadística. 1990. Censo nacional de poblacion.

  21. American Association of Clinical Endocrinologists (AACE). AACE Lipid Guidelines. (2000) Endocr. Pract. 6:164-213.

  22. Wood, D., De Backer, G., Faergeman, O., Graham, I., Mancia, G., Pyörälä, K., together with members of the Task Force,. 1998. Prevention of coronary heart disease in clinical practice: recommendations of the Second Joint Task Force of European and other Societies on Coronary Prevention. Atherosclerosis. 140:199-270[Medline].

  23. National Cholesterol Education Program. Second report of the Expert Panel on detection, evaluation and treatment of high blood cholesterol in adults. (1994) Circulation. 89:1329-1445.

  24. Recommendations of the European Atherosclerosis Society prepared by the International Task Force for Prevention of Coronary Heart Disease. Prevention of coronary heart disease. Scientific background and new clinical guidelines. (1992) Nutr. Metab. Cardiovasc. Dis. 2:113-156.

  25. Taniguchi, A., Fukushima, M., Sakai, M., Kataoka, K., Nagata, I., Doi, K., Arakawa, H., Nagasaka, S., Tokuyama, K., Nakai, Y. 2000. The role of body mass index and triglycerides levels in identifying insulin-sensitive and insulin-resistant variants in Japanese non-insulin dependent diabetic patients. Metabolism. 49:1001-1005[Medline].

  26. Mahley, R. W., Erhan-Palaoglu, K., Atak, Z., Dawson-Pepin, J., Langlois, A. M., Cheung, V., Onat, H., Fulks, P., Mahley, L., Vakar, F., Özbayrakci, S., Gökdemir, O., Winkler, W. 1995. Turkish heart study: lipids, lipoproteins and apolipoproteins. J. Lipid Res. 36:839-859[Abstract].

  27. Bhopal, R., Unwin, N., White, M., Yallop, J., Walker, L., Alberti, K. G. M. M., Harland, J., Patel, S., Ahmad, N., Turner, C., Watson, B., Kaur, D., Kulkarni, A., Laker, M., Tavridou, A. 1999. Heterogeneity of coronary heart disease risk factors in Indian, Pakistani, Bangladeshi, and European origin populations: cross sectional study. BMJ. 319:215-220[Abstract/Free Full Text].

  28. Lavalle, C., Alarcón-Segovia, D., Del Giudice-Knipping, J. A., Fraga, A. 1981. Association of Behcet's syndrome with HLA-B5 in the Mexican mestizo population. J. Rheumatol. 8:325-327[Medline].

  29. Mahley, R. W., Pepin, J., Palaoglu, K. E., Malloy, M. J., Kane, J. P., Bersot, T. P. 2000. Low levels of high density lipoproteins in Turks, a population with elevated hepatic lipase. High density lipoprotein characterization and gender-specific effects of apolipoprotein E genotype. J. Lipid Res. 41:1290-1301[Abstract/Free Full Text].

  30. Dixon, L. B., Sudquist, J., Winkleby, M. 2000. Differences in energy, nutrient and food intakes in a US sample of Mexican American women and men: findings from the Third National Health and Nutrition Examination Survey, 1988;–1994. Am. J. Epidemiol. 152:548-557[Abstract/Free Full Text].

  31. Loria, C., Bus, T., Carroll, M., Looker, A., McDowell, M., Johnson, C., Sempos, C. 1995. Macronutrient intakes among adult Hispanics: a comparison of Mexican Americans, Cuban Americans, and Mainland Puerto Ricans. Am. J. Public Health. 85:684-689[Abstract/Free Full Text].

  32. Parks, E. J., Hellerstein, M. K. 2000. Carbohydrate induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms. Am. J. Clin. Nutr. 71:412-433[Abstract/Free Full Text].

  33. Asztalos, B., Lefevre, M., Wong, L., Foster, T., Tulley, R., Windhauser, M., Zhang, W., Roheim, P. 2000. Differential response to low fat diet between low and normal HDL cholesterol subjects. J. Lipid Res. 41:321-328[Abstract/Free Full Text].

  34. Saku, K., Zhang, B., Shirai, K., Jimi, S., Yoshinaga, K., Arakawa, K. 1999. Hyperinsulinemic hypoalphalipoproteinemia as a new indicator for coronary heart disease. J. Am. Coll. Cardiol. 34:1443-1451[Abstract/Free Full Text].

  35. Brinton, E. A., Eisenberg, S., Breslow, J. L. 1990. A low fat diet decreases high density lipoprotein cholesterol levels by decreasing HDL apolipoprotein transport rates. J. Clin. Invest. 85:144-151.

  36. National Center for Health Statistics. Plan and operation of the Third National Health and Nutrition Examination Survey 1988;–1994. (1994) Vital Health Stat. 1:32.

  37. Mitchell, B. D., Gonzalez-Villalpando, C., Arredondo-Perez, B., Garcia, M. S., Valdez, R., Stern, M. P. 1995. Myocardial infarction and cardiovascular risk factors in Mexico City and San Antonio, Texas. Arterioscler. Thromb. Vasc. Biol. 15:721-725[Abstract/Free Full Text].

  38. Gonzalez-Villalpando, C., Stern, M. P., Haffner, S. M., Gonzalez Villapando, M. E., Gaskill, S., Rivera-Martinez, D. 1999. Prevalence of hypertension in a Mexican population according to the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. J. Cardiovasc. Risk. 6:177-181[Medline].

  39. Oberman, A. 2000. Hypertriglyceridemia and coronary heart disease. J. Clin. Endoc. Metab. 85:2098-2105[Free Full Text].

  40. Austin, M., Hokanson, J. E., Edwards, K. 1998. Hypertriglyceridemia as a cardiovascular risk factor. Am. J. Cardiol. 81(4A):7B-12B[Medline].

  41. Assmann, G., and H. Schulte. 1993. Results and conclusions of the Prospective Cardiovascular Münster (PROCAM) Study. In Lipid Metabolism Disorders and Coronary Heart Disease. G. Assmann, editor. MMV Medizin Verlag. 21;–67.

  42. Schonfeld, G., Aguilar-Salinas, C., Elias, N. 1998. Role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ("statins") in familial combined hyperlipidemia. Am. J. Cardiol. 81(4A):43B-46B[Medline].

  43. Betteridge, J., Khan, M. 1995. Review of the guidelines for management of dislipidemia. Ballerie's Clin. Endocrinol. and Metabol. 9:867-890.

  44. Gaw, A. 1998. Evidence based approach for the management of mixed hyperlipidemia. Atherosclerosis. 137(Suppl.):S97-S100.

  45. Hyperlipoproteinemia, F. C. 1999. Experts panel position on diagnostic criteria for clinical practice. Committee of experts of the Atherosclerosis and Dysmetabolic Disorders Study Group. Nutr. Metab. Cardiovasc. Dis. 9:304-311[Medline].

  46. Gómez-Pérez, F. J., J. Salmeron, C. A. Aguilar-Salinas, A. Frati, E. García, and I. Lerman. 1999. Diabetes mellitus. In Diez Problemas Relevantes de Salud Pública en México. Fondo de Cultura Económica, editors. 1st edition. 167;–186.

  47. Santamarina, F. S. 1998. The Familial Chylomicronemia syndrome. Endocrinol. Metab. Clin. North Am. 27:551-567[Medline].

  48. Garg, A. 1998. Treatment of diabetic dyslipidemia. Am. J. Cardiol. 81(4A):47B-51B[Medline].

  49. Brunzell, J. D., Hokanson, J. E. 1999. Dyslipidemia of central obesity and insulin resistance. Diabetes Care. 22(Suppl. 3):C10-13.

  50. Adam, B., Talu, C., Bedir, A., Alvur, M., Sagkan, O. 1999. The levels of lipids, lipoproteins and apolipoproteins in healthy people in the central region of the Black Sea. Jpn. Heart J. 40:427-434[Medline].

  51. Assmann, G., Schulte, H. 1992. Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerosis coronary artery disease. (The PROCAM experience). Am. J. Cardiol. 70:733-738[Medline].

  52. Centers for Disease Control and Prevention. National Center for Health Statistics. NHANES III. 1988;–1991.

  53. Fong, P. C., Tam, S. C., Tai, Y., Lau, C., Lee, J., Sha, Y. 1994. Serum lipid and apolipoprotein distribution in Hong Kong Chinese. J. Epidemiol. Community Health. 48:355-359[Abstract].

  54. Leino, A., Impivaara, O., Kaitsaari, M., Jarvisalo, J. 1995. Serum concentrations of apolipoprotein A-I, apolipoprotein B and lipoprotein (a) in a population sample. Clin. Chem. 41:1633-1636[Abstract/Free Full Text].


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 DiabetesHome page
M. T. Villarreal-Molina, C. A. Aguilar-Salinas, M. Rodriguez-Cruz, D. Riano, M. Villalobos-Comparan, R. Coral-Vazquez, M. Menjivar, P. Yescas-Gomez, M. Konigsoerg-Fainstein, S. Romero-Hidalgo, et al.
The ATP-Binding Cassette Transporter A1 R230C Variant Affects HDL Cholesterol Levels and BMI in the Mexican Population: Association With Obesity and Obesity-Related Comorbidities
Diabetes, July 1, 2007; 56(7): 1881 - 1887.
[Abstract] [Full Text] [PDF]

Home page
 Diabetes CareHome page
C. A. Aguilar-Salinas, R. Rojas, C. Gonzalez-Villalpando, F. J. Gomez-Perez, R. Mehta, G. Olaiz, J. A. Rull, and D. R. Cox
Design and validation of a population-based definition of the metabolic syndrome.
Diabetes Care, November 1, 2006; 29(11): 2420 - 2426.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart J SupplHome page
E. Bruckert
Epidemiology of low HDL-cholesterol: results of studies and surveys
Eur. Heart J. Suppl., October 1, 2006; 8(suppl_F): F17 - F22.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
A. Huertas-Vazquez, C. Aguilar-Salinas, A. J. Lusis, R. M. Cantor, S. Canizales-Quinteros, J. C. Lee, L. Mariana-Nunez, R.-M. L. Riba-Ramirez, A. Jokiaho, T. Tusie-Luna, et al.
Familial Combined Hyperlipidemia in Mexicans: Association With Upstream Transcription Factor 1 and Linkage on Chromosome 16q24.1
Arterioscler. Thromb. Vasc. Biol., September 1, 2005; 25(9): 1985 - 1991.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart J SupplHome page
E. Bruckert, R. Pamphile, F. McCoy, and P. Andre
Defining the prevalence of low HDL-C in a European cohort of dyslipidaemic patients
Eur. Heart J. Suppl., July 1, 2005; 7(suppl_F): F23 - F26.
[Abstract] [Full Text] [PDF]

Home page
 Diabetes CareHome page
A. Jimenez-Cruz and M. Bacardi-Gascon
The Fattening Burden of Type 2 Diabetes on Mexicans: Projections from early growth to adulthood
Diabetes Care, May 1, 2004; 27(5): 1213 - 1215.
[Full Text] [PDF]

Home page
 Diabetes CareHome page
C. A. Aguilar-Salinas, O. V. Monroy, F. J. Gomez-Perez, A. G. Chavez, A. L. Esqueda, V. M. Cuevas, J. A. Rull-Rodrigo, and R. T. Conyer
Characteristics of Patients With Type 2 Diabetes in Mexico: Results from a large population-based nationwide survey
Diabetes Care, July 1, 2003; 26(7): 2021 - 2026.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. Canizales-Quinteros, C. A. Aguilar-Salinas, E. Reyes-Rodriguez, L. Riba, M. Rodriguez-Torres, S. Ramirez-Jimenez, A. Huertas-Vazquez, V. Fragoso-Ontiveros, A. Zentella-Dehesa, J. L. Ventura-Gallegos, et al.
Locus on Chromosome 6p Linked to Elevated HDL Cholesterol Serum Levels and to Protection Against Premature Atherosclerosis in a Kindred With Familial Hypercholesterolemia
Circ. Res., March 21, 2003; 92(5): 569 - 576.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Aguilar-Salinas, C. A.
Right arrow Articles by Sepulveda, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Aguilar-Salinas, C. A.
Right arrow Articles by Sepulveda, J.
Social Bookmarking