Author: admin

Breastfeeding during the first 4 to 6 months of life was associated with a lower central precocious puberty (CPP) risk in boys and girls, according to a nationwide, retrospective cohort study published in JAMA Network Open.¹

Pubertal age onset has declined over recent decades, having decreased by by a mean of nearly 3 months per decade from 1977 to 2013.² Accompanying the decline has been a rising incidence of CPP globally, which is associated with an increased risk of adult health issues, such as cardiovascular disease, diabetes, and cancer.¹

“Human milk is the first source of nutrition that newborns receive immediately after birth and usually serves as the sole source of nutrition during the first 4 to 6 months of life before complementary foods are introduced,” wrote the study authors. The World Health Organization recommends breastfeeding exclusivity for the first 6 months of life and continued feeding with complementary foods for up to 2 years of age.

Prepubertal obesity, the authors wrote, is thought to affect pubertal development differently among boys and girls, with multiple studies having already investigated these associations based on sex. However, mechanisms underlying the differences in adiposity-related pubertal development remain unclear.

“This study investigated the association between primary feeding type during the first 4 to 6 months of life and the risk of CPP in South Korea. Additionally, we explored whether being overweight or obese during the prepubertal period mediates this association,” wrote the authors.

The main outcome of the study was the incidence of CPP. The association between feeding practices and incidence of CPP was assessed using a multivariable Cox proportional hazards model to estimate adjusted hazard ratios (AHRs) and 95% CIs.

Of the 322,731 children included in the retrospective study (58.1% female), 46% were exclusively breastfed and 34.9% were formula-fed, with 19.1% mixed-fed. Compared to exclusively breastfed children, those who were formula-fed had a great risk of CPP in boys (adjusted hazard ratio [AHR], 1.16; 95% CI, 1.10-1.21 [P < .001]) and girls (AHR, 1.60; 95% CI, 1.24-2.06 [P < .001]). Mixed-fed had the next highest risk, with AHR in boys of 1.14 (95% CI, 1.07-1.20) and 1.45 in girls (95% CI, 1.07-1.97 [P < .001]).

Kaplan-Meier survival curves demonstrated significant differences in the cumulative incidence of CPP by primary feeding type among both sexes. The lowest risk observed was among children who were exclusively breastfed (log-rank P < .001). Additionally, low birth weight was significantly associated with increased CPP risk in boys and girls (AHR, 1.99; 95% CI, 1.21-3.26; [P = .007]; AHR, 1.17; 95% CI, 1.05-1.30; [P = .003]). Prepubertal overweight or obesity partially mediated the association between primary feeding type and CPP in both boys and girls.

This study had several limitations, the authors noted, including the lack of maternal age at menarche data and the inclusion of only children treated with GnRH agonists under the insurance reimbursement system, which may have led to potential overdiagnosis of CPP, though diagnostic criteria helped mitigate this concern. The study also could not examine dose-dependent effects of breastfeeding duration, distinguish between bottle-fed and directly breastfed infants, or fully account for temporal variability in overweight or obesity since it was modeled as a fixed covariate. Finally, the observational design prevents causal inference due to the possibility of unmeasured or residual confounding.

While concluding that exclusive breastfeeding in early infancy was linked to a lower CPP risk in boys and girls, “further longitudinal prospective studies are needed to evaluate the association of breastfeeding with pubertal timing and progression,” stated the study authors.

References:

1. Choe Y, Ryu S, Choi J, et al. Breastfeeding, Prepubertal Adiposity, and Development of Precocious Puberty. JAMA Netw Open. 2025;8(8):e2527455. doi:10.1001/jamanetworkopen.2025.27455
2. Eckert-Lind C, Busch AS, Petersen JH, et al. Worldwide secular trends in age at pubertal onset assessed by breast development among girls: a systematic review and meta-analysis. JAMA Pediatr. 2020;174(4):e195881. doi:10.1001/jamapediatrics.2019.5881

These findings collectively suggest that low vitamin D levels may represent a significant and underrecognised risk factor for cardiovascular disease.

Synopsis: A study found that people with low vitamin D levels are nearly six times more likely to suffer from coronary artery disease (CAD), one of the leading causes of death in the country. The new research employed a robust case-control design, recruiting 250 patients with confirmed coronary artery disease and comparing them to 260 healthy individuals of similar age and background who served as controls.

An Indian study has unveiled alarming findings about the relationship between vitamin D deficiency and heart disease. It revealed that people with low vitamin D levels are nearly six times more likely to suffer from coronary artery disease (CAD), one of the leading causes of death in the country.

The research, published in the Indian Journal of Medical Research, also suggests that certain genetic variations may influence whether vitamin D deficiency leads to a higher risk of heart disease.

The study was conducted by scientists from Sri Jayadeva Institute of Cardiovascular Sciences and Research in Bengaluru, Sri Ramachandra Institute of Higher Education and Research in Chennai, and the National Institute of Mental Health and Neuro Sciences (NIMHANS).

Coronary artery disease, which occurs when the arteries supplying blood to the heart become narrow or blocked, has emerged as a significant health crisis in India, responsible for nearly 27 percent of all medically certified deaths in the country.

What makes this particularly concerning is that, unlike in Western countries, Indians tend to develop CAD at a much younger age, often a decade earlier, striking people in their most productive years.

Healthcare professionals have long attributed this phenomenon to a complex interplay of traditional risk factors, including diabetes, high blood pressure, smoking, and high cholesterol, combined with genetic susceptibility and lifestyle changes. However, the role of vitamin D deficiency has come under increasing focus in recent years as researchers seek to understand the underlying mechanisms driving India’s heart disease epidemic.

Also Read: Vitamin D deficiency may directly cause erectile dysfunction

The sunshine vitamin’s hidden role

Vitamin D, popularly called the “sunshine vitamin,” is produced in the body when skin is exposed to sunlight.

While it is well-known for its role in maintaining bone strength, researchers over the last two decades have discovered that vitamin D also plays a crucial role in regulating blood pressure, controlling blood sugar, and reducing inflammation — all key processes linked to heart disease.

Despite India being a tropical country with abundant sunlight, vitamin D deficiency has reached epidemic proportions.

Studies suggest that anywhere between 50 percent and 90 percent of Indians have insufficient levels, a paradox explained by indoor lifestyles, increasing pollution levels, traditional clothing patterns that cover most of the skin, and dietary patterns that provide little vitamin D.

Vitamin D and CAD

The new research employed a robust case-control design, recruiting 250 patients with confirmed coronary artery disease and comparing them to 260 healthy individuals of similar age and background who served as controls. Blood samples were systematically collected to measure vitamin D levels, and sophisticated genetic tests were carried out to examine differences in the vitamin D receptor (VDR) gene.

The VDR gene produces a protein that acts as a biological “lock” into which vitamin D fits like a “key.” Once this receptor is activated, it switches on or off several other genes that influence critical processes in the heart, blood vessels, and immune system. The researchers specifically examined four commonly studied VDR variants — called ApaI, BsmI, FokI, and TaqI — named after the specialised enzymes used to identify them in laboratory settings.

The study’s findings painted a concerning picture of vitamin D deficiency’s impact on cardiovascular health. A staggering 90 percent of CAD patients demonstrated vitamin D deficiency, defined as less than 20 nanograms per millilitre of blood, compared to 63 percent of healthy controls.

The severity of deficiency was equally alarming, with CAD patients averaging vitamin D levels of just 12 ng/ml, while the healthy group maintained levels of 18 ng/ml.

Most significantly, people with very low vitamin D levels (below 20 ng/ml) were 5.7 times more likely to have heart disease than those with healthier levels, representing one of the strongest associations documented in Indian populations.

Interestingly, while vitamin D is theoretically understood to affect blood pressure and blood sugar regulation, this study did not find any direct link between vitamin D levels and those specific factors.

However, researchers observed a weak negative trend suggesting that individuals with higher vitamin D levels tended to have slightly lower cholesterol and triglyceride levels, though these results were not strong enough to be considered conclusive.

The genetic analysis component of the study produced particularly nuanced and surprising results, demonstrating that not all genetic variants affected disease risk equally, and in some cases, gender played a significant determining role in outcomes.

Broader context and global perspective

The researchers placed their findings within a broader international context, noting that vitamin D deficiency and insufficiency are considered a global pandemic, affecting approximately 50 percent of the world’s population. In India specifically, the prevalence of vitamin D deficiency ranges from 50-94 percent, making it one of the most widespread nutritional deficiencies in the country.

“In a meta-analysis of 44,717 participants across 65 studies from five South Asian countries, including India, Pakistan, Bangladesh, Nepal, and Sri Lanka, the prevalence of VDD was 67 percent among Indians. The average level of vitamin D ranged from 4.7 to 32 ng/ml, with a weighted mean of 19.15 ng/ ml,” the researchers documented.

The study also referenced international research, noting that “a meta-analysis by Yan et al, which included 13 studies from China, Iran, Brazil, Egypt, Poland, Croatia, and Germany, concluded that low plasma vitamin D levels are associated with CAD.”

Previous research from Northern India had documented similarly concerning patterns, with “a study from the Northern part of India on first incident acute myocardial infarction reported a higher prevalence of VDD and insufficiency and much lower mean values of vitamin D (98.3% of the cases had below normal values with a mean level of 6 ng/ml; 95.8% of controls had below normal values with a mean of 11.1 ng/ml). A 4.5-fold risk of myocardial infarction was also noted among individuals with severe (<10 ng/ml) VDD.”

These findings collectively suggest that low vitamin D levels may represent a significant and underrecognised risk factor for cardiovascular disease, particularly in populations with a high prevalence of vitamin D deficiency, like India.

Also Read: Why India is short on vitamin D

Expert perspective on study limitations

Despite the compelling associations revealed by the study, medical experts urge caution in interpreting the results. Dr Sudhir Kumar, Senior Consultant Neurologist at Apollo Hospitals, Hyderabad, provided important context about the study’s limitations and the broader body of evidence.

“See, there are two things. This is a case-control study, and such studies are the weakest form of research. They can show an association but cannot prove cause and effect. To prove causation, we need randomised controlled trials, and ideally meta-analyses that pool data from many such trials. On this topic, over the past 10 years, several randomised trials have been done worldwide, and none of them showed that vitamin D deficiency directly causes heart disease,” Dr Kumar explained.

He emphasised the distinction between correlation and causation, noting that “when it comes to case-control or observational studies, many have been done in India and abroad. Almost all of them show a correlation — that people with heart disease often also have vitamin D deficiency. But correlation is not causation. Based on this study, we can say that the two are linked, but we cannot say vitamin D deficiency causes coronary artery disease.”

Dr Kumar highlighted a critical methodological concern that affects the interpretation of such studies. “There’s also the issue of confounding factors. For example, people with heart disease often become less physically active years before diagnosis. Less activity means less sunlight exposure, which naturally lowers vitamin D. They may also be obese or have arthritis—conditions that keep them indoors. These factors can lower vitamin D without vitamin D itself being the cause of heart disease. A case-control study cannot fully account for this,” he explained.

This observation points to the complex web of lifestyle factors that can simultaneously influence both vitamin D levels and cardiovascular health, making it challenging to establish direct causal relationships through observational studies alone.

Dr Kumar provided practical guidance for healthcare practitioners and the public, emphasising evidence-based recommendations. “That is why randomised controlled trials are so important. Fortunately, many have been done, and they show no causal link. Whether people received vitamin D supplements or not, the rates of heart disease were the same. So, we should be clear with the public: If someone has low vitamin D, it should be corrected, but the goal is better bone and muscle health — not heart protection.”

(Edited by Muhammed Fazil.)