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The impact of diabetes mellitus type 1 on male fertility: Systematic review and meta-analysis.
Facondo, P, Di Lodovico, E, Delbarba, A, Anelli, V, Pezzaioli, LC, Filippini, E, Cappelli, C, Corona, G, Ferlin, A
Andrology. 2022;10(3):426-440
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The relationship between type 2 diabetes mellitus and male hypogonadism is well known, whereas the impact of type 1 diabetes mellitus (DM1) on male fertility and testis functions has been less studied. The aim of this study was to systematically review and discuss the available evidence evaluating paternity rate, male gonadal axis, and sperm parameters in men with DM1. This study is a systematic review and meta-analysis of fourteen studies. Results show: - reduced fertility potential in patients with DM1, as they have a lower number of children compared with unaffected population. In fact, the rate of children is statistically significantly lower among men who had been diagnosed with DM1 at an earlier age, according to a longer duration of the disease. - that men with DM1, compared with controls, have significantly lower normal sperm morphology, progressive motility and a trend toward a reduced semen volume, without difference in total sperm count and concentration. Authors conclude that DM1 might impair reproductive health at different levels, including functional sperm alterations definitively leading to reduced fertility rate in these patients.
Abstract
BACKGROUND Some evidence suggests that diabetes mellitus type 1 (DM1) could affect male fertility, gonadal axis, semen parameters, and spermatogenesis because of effects of hyperglycemia and insulin deficiency. Anyhow, the exact impact of DM1 on male fertility is unclear. OBJECTIVES To review the studies evaluating paternity rate, male gonadal axis, and semen parameters in men with DM1. MATERIALS AND METHODS A review of relevant literature from January 1980 to December 2020 was performed. Only studies published in English reporting data on fatherhood (rate of children by natural fertility), hormonal and seminal parameters were included. Out of 14 retrieved articles, the eight studies evaluating semen parameters were meta-analyzed. RESULTS The rate of children (four studies) was lower than controls among men affected by DM1, especially in men with a longer duration of disease. The data of gonadal hormonal profile in DM1 men (six studies) are very heterogeneous and a neutral effect of DM1 or a condition of subclinical hypogonadism could not be concluded. Meta-analysis showed that men with DM1 (n = 380), compared with controls (n = 434), have significantly lower normal sperm morphology [-0.36% (-0.66; -0.06), p < 0.05, six studies] and sperm progressive motility [33.62% (-39.13; -28.11), p < 0.001, two studies] and a trend toward a lower seminal volume [-0.51 (-1.03; 0.02), p = 0.06, eight studies], without difference in total sperm count and concentration. Data on scrotal ultrasound and sperm DNA fragmentation are too few. No study evaluated other factors of male infertility, such as transrectal ultrasound, semen infections, sperm auto-antibodies, and retrograde ejaculation. DISCUSSION DM1 might impair male fertility and testis functions (endocrine, spermatogenesis), but definition of its actual impact needs further studies. CONCLUSION Men with DM1 should be evaluated with a complete hormonal, seminal, and ultrasound workup to better define their fertility potential and need for follow up of testis functions.
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Dietary macronutrients and the gut microbiome: a precision nutrition approach to improve cardiometabolic health.
Jardon, KM, Canfora, EE, Goossens, GH, Blaak, EE
Gut. 2022;71(6):1214-1226
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The global rise in the prevalence of obesity is strongly associated with an increase in the incidence and prevalence of cardiometabolic diseases, including insulin resistance (IR) and type 2 diabetes mellitus. In recent years, advancements have been made in understanding the involvement of the gut microbiome in obesity and related cardiometabolic complications as regulator of host energy and substrate metabolism. This study is a review that discusses the latest research describing interactions between dietary composition, the gut microbiome and host metabolism. Results show that current evidence for developing optimal dietary interventions targeting bodyweight control and IR via the gut microbiota is still in its infancy and does not capture the complexity of the integration of a whole-diet approach, the microbial and the host’s metabolic phenotype. Furthermore, implementation of targeted, precision nutrition intervention strategies or dietary guidelines for individuals or subgroups in public health requires further insight in the mechanisms involved in (non-)response to dietary intervention. Authors conclude that future studies are needed and these should focus on assessing detailed individual phenotyping and gaining insight into the balance between carbohydrate and protein fermentation by the gut microbiota as well as the site of fermentation in the colon.
Abstract
Accumulating evidence indicates that the gut microbiome is an important regulator of body weight, glucose and lipid metabolism, and inflammatory processes, and may thereby play a key role in the aetiology of obesity, insulin resistance and type 2 diabetes. Interindividual responsiveness to specific dietary interventions may be partially determined by differences in baseline gut microbiota composition and functionality between individuals with distinct metabolic phenotypes. However, the relationship between an individual's diet, gut microbiome and host metabolic phenotype is multidirectional and complex, yielding a challenge for practical implementation of targeted dietary guidelines. In this review, we discuss the latest research describing interactions between dietary composition, the gut microbiome and host metabolism. Furthermore, we describe how this knowledge can be integrated to develop precision-based nutritional strategies to improve bodyweight control and metabolic health in humans. Specifically, we will address that (1) insight in the role of the baseline gut microbial and metabolic phenotype in dietary intervention response may provide leads for precision-based nutritional strategies; that (2) the balance between carbohydrate and protein fermentation by the gut microbiota, as well as the site of fermentation in the colon, seems important determinants of host metabolism; and that (3) 'big data', including multiple omics and advanced modelling, are of undeniable importance in predicting (non-)response to dietary interventions. Clearly, detailed metabolic and microbial phenotyping in humans is necessary to better understand the link between diet, the gut microbiome and host metabolism, which is required to develop targeted dietary strategies and guidelines for different subgroups of the population.
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Improvement of Inflammation and Pain after Three Months' Exclusion Diet in Rheumatoid Arthritis Patients.
Guagnano, MT, D'Angelo, C, Caniglia, D, Di Giovanni, P, Celletti, E, Sabatini, E, Speranza, L, Bucci, M, Cipollone, F, Paganelli, R
Nutrients. 2021;13(10)
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Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease typically affecting the synovial joints, in which autoimmunity drives dysregulated proinflammatory cytokine secretion. A decrease in dietary fibres and an increase in fat and sugar intake, which is typical in Western diets, contributes to gut microbial dysbiosis, leading to immune dysfunction. In fact, the changes in the gastrointestinal microbiota are thought to influence the pathogenesis and progression of RA. The aim of this diet was to investigate the effect of a diet deprived of meat, gluten, and lactose (excluding all dairy products and foods containing them) in patients with long-standing, well-controlled RA, in comparison with a control balanced diet including those items, followed for three months. This study is a randomised controlled study. All participants (n=40) were females with ages ranging between 31 and 72 years. They were randomly assigned to one of the two experimental groups and asked to follow a diet excluding meat, gluten and lactose (group A) or a balanced diet (group B). Results show that: - exclusion of meat, gluten and lactose, all of which reported as suspected of worsening of symptoms in RA, with the inclusion of fish, may carry additional health benefits to overweight patients compared with those obtained by a standard weight-reduction program (group B). - both diets, despite not affecting the disease activity, tended to reduce the arthritic pain perception and to improve the quality of life of the patients. - metabolic and inflammatory parameters showed a trend to normalise. - the immunological correlates of RA were not sensitive to either diet. Authors conclude that prevention of complications of RA might be better achieved by the exclusion diet. Thus, a diet prescription should be included in therapeutic plans for RA.
Abstract
INTRODUCTION Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease affecting the synovial joints and causing severe disability. Environmental and lifestyle factors, including diet, have been proposed to play a role in the onset and severity of RA. Dietary manipulation may help to manage the symptoms of RA by lowering inflammation and potentially decreasing pain. METHODS In 40 patients with long-standing RA with stable symptoms and treated with conventional (c-) and biological (b-) disease modifying anti-rheumatic drugs (DMARDs), the effect of a 3-month diet avoiding meat, gluten, and lactose (and all dairy products; privative diet) was evaluated in comparison with a control balanced diet including those foods. Both diets were designed to reduce weight since all patients were overweight or obese. Patients were randomly assigned to one of the diets, and RA was clinically assessed at Time 0 (T0), through the Visual Analogue Scale (VAS), for pain, and the Disease Activity Score of 28 joints (DAS 28) for RA activity. Patients were also administered the Short Form Health survey (SF-36) and the Health Assessment Questionnaire (HAQ). At T0, a blood sample was collected for laboratory tests and adipokines measurements, and anthropometric measurements were compared. These evaluations were repeated at the end of the 3 months' dietary regimens. RESULTS A significant decrease in VAS and the improvement of the overall state of physical and mental health, assessed through SF-36, was observed in patients assigned to the privative diet. Both dietary regimens resulted in the improvement of quality of life compared to baseline values; however, the change was significant only for the privative diet. With either diet, patients showed significant decreases in body weight and body mass index, with a reduction in waist and hips circumference and lower basal glucose and circulating leptin levels. A privative diet was also able to significantly reduce systolic (p = 0.003) and diastolic (p = 0.025) arterial pressure. The number of circulating leukocytes and neutrophils, and the level of hs-C-Reactive Protein also decreased after 3 months of the meat-, lactose-, and gluten-free diet. CONCLUSIONS Our results suggest that a privative diet can result in a better control of inflammation in RA patients under stable optimized drug treatment.
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Anti-aging Effects of Calorie Restriction (CR) and CR Mimetics based on the Senoinflammation Concept.
Kim, DH, Bang, E, Jung, HJ, Noh, SG, Yu, BP, Choi, YJ, Chung, HY
Nutrients. 2020;12(2)
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Low grade, systemic, chronic inflammation is a feature of ageing and underlies many age-related chronic diseases states. As cells age their capacity to proliferate declines, which is referred to as cell senescence. Such senescent cells release multiple inflammatory markers contributing to a pro-inflammatory state. This is further aggravated by elevated oxidative stress and a reduced capacity to manage it, eventually leading to improper gene regulation and DNA damage. To define this age-related, complex inflammatory phenomena the authors introduced the term senoinflammation. A well-established intervention to reverse or slow down the ageing process and many ageing-associated diseases is calorie restriction (CR), by means of reducing overall caloric intake without malnutrition. CR exhibits potent anti-inflammatory effects, reduces age-associated oxidative stress, improves age-related metabolic dysregulation and enhances favourable gene expression. This review summarises how CR and CR-mimicking substances exert their anti-inflammatory effect and some of the cellular mechanism involved and may be of interest to those who are looking to get a more detailed understanding on ageing, inflammation and the benefits of CR.
Abstract
Chronic inflammation, a pervasive feature of the aging process, is defined by a continuous, multifarious, low-grade inflammatory response. It is a sustained and systemic phenomenon that aggravates aging and can lead to age-related chronic diseases. In recent years, our understanding of age-related chronic inflammation has advanced through a large number of investigations on aging and calorie restriction (CR). A broader view of age-related inflammation is the concept of senoinflammation, which has an outlook beyond the traditional view, as proposed in our previous work. In this review, we discuss the effects of CR on multiple phases of proinflammatory networks and inflammatory signaling pathways to elucidate the basic mechanism underlying aging. Based on studies on senoinflammation and CR, we recognized that senescence-associated secretory phenotype (SASP), which mainly comprises cytokines and chemokines, was significantly increased during aging, whereas it was suppressed during CR. Further, we recognized that cellular metabolic pathways were also dysregulated in aging; however, CR mimetics reversed these effects. These results further support and enhance our understanding of the novel concept of senoinflammation, which is related to the metabolic changes that occur in the aging process. Furthermore, a thorough elucidation of the effect of CR on senoinflammation will reveal key insights and allow possible interventions in aging mechanisms, thus contributing to the development of new therapies focused on improving health and longevity.
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Associations of Meal Timing and Frequency with Obesity and Metabolic Syndrome among Korean Adults.
Ha, K, Song, Y
Nutrients. 2019;11(10)
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The timing of food intake appears to affect the robustness of circadian rhythms in metabolic organs, and circadian rhythm disruption is emerging as a new risk factor for cardiovascular disease. As major risk factors for cardiovascular diseases, obesity and metabolic syndrome are critical worldwide issues. In Korea, 3 in 10 adults have obesity or the metabolic syndrome. The aim of this study was to explore meal timing and frequency using various variables, including nightly fasting duration and specific time periods such as morning and night, and to examine their associations with obesity and metabolic syndrome in Korean adults using national survey data. The study used data from the 2013–2017 Korea National Health and Nutrition Examination Survey (KNHANES), which is a continuous annual survey conducted by the Korea Centers for Disease Control and Prevention Results indicated that a greater number of eating episodes was associated with lower prevalence of metabolic abnormalities in men. Furthermore, the prevalence of metabolic syndrome was inversely associated with morning eating in both men and women, whereas it was positively associated with night eating in men. Authors conclude that having desirable eating patterns, including eating in the morning and avoiding eating after 21:00, and an appropriate sleep schedule may be helpful for reducing the risks of obesity and metabolic syndrome, independently of fasting duration.
Abstract
Emerging studies indicate that meal timing is linked to cardiometabolic risks by deterioration of circadian rhythms, however limited evidence is available in humans. This large-scale cross-sectional study explored the associations of meal timing and frequency with obesity and metabolic syndrome among Korean adults. Meal timing was defined as nightly fasting duration and morning, evening, and night eating, and meal frequency was estimated as the number of daily eating episodes using a single-day 24-hour dietary recall method. Meal frequency was inversely associated with prevalence of abdominal obesity, elevated blood pressure, and elevated triglycerides in men only. Independent of the nightly fasting duration and eating episodes, morning eating was associated with a lower prevalence of metabolic syndrome (odds ratio (OR), 0.73; 95% confidence interval (CI), 0.57-0.93 for men and OR, 0.69; 95% CI, 0.54-0.89 for women) than no morning eating, whereas night eating was associated with a 48% higher prevalence of metabolic syndrome (OR, 1.48; 95% CI, 1.15-1.90) than no night eating in men only. Longer fasting duration and less sleep were associated with obesity and metabolic syndrome. These findings suggest that overall eating patterns, including energy distribution across the day, eating frequency, and sleep duration, rather than fasting duration alone, are related to cardiometabolic risks in free-living Korean adults.
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Functional interactions between the gut microbiota and host metabolism.
Tremaroli, V, Bäckhed, F
Nature. 2012;489(7415):242-9
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This literature review aims to discuss evidence for the role of the gut microbiota in metabolism and possible links to obesity. Obesity and caloric intake can influence the microbiota, but whether the reverse is true in humans remains unclear. Much of the mechanisms have been determined in rodents, determining similar pathways in humans is difficult. The interplay of diet, host and gut microbiota may cause increased gut permeability (leaky gut) that could lead to an increase in inflammation that may cause obesity, fatty liver disease and insulin resistance. It is increasingly accepted that gut microbiota can contribute to diseases such as obesity, diabetes and cardiovascular disease, but exactly how and by how much remains unclear. Evidence for treating the microbiota to help with these metabolic diseases, either by pre- or probiotic supplementation, is building. However, double-blind, placebo-controlled studies are required to determine effects. The influence of the gut microbiota is a promising area, but one that needs further research.
Abstract
The link between the microbes in the human gut and the development of obesity, cardiovascular disease and metabolic syndromes, such as type 2 diabetes, is becoming clearer. However, because of the complexity of the microbial community, the functional connections are less well understood. Studies in both mice and humans are helping to show what effect the gut microbiota has on host metabolism by improving energy yield from food and modulating dietary or the host-derived compounds that alter host metabolic pathways. Through increased knowledge of the mechanisms involved in the interactions between the microbiota and its host, we will be in a better position to develop treatments for metabolic disease.
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Role of early hormonal and nutritional experiences in shaping feeding behavior and hypothalamic development.
Bouret, SG
The Journal of nutrition. 2010;140(3):653-7
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Obesity in children and adults is increasingly becoming a serious health problem, particularly in Western countries. The precise biological mechanisms underlying the disease are not clear, and it is equally unclear why certain individuals are more predisposed than others. Research suggests that the perinatal conditions and periods of organ development may predispose individuals to obesity later in life. For example, maternal malnutrition, diabetes and/or obesity during pregnancy can increase susceptibility to obesity. The hypothalamus, the region of the brain associated with feeding and glucose homeostasis, develops primarily in utero and is thought to be influenced by hormones such as leptin, ghrelin and insulin that may indicate nutrient availability in the environment. Imbalances in these hormones therefore may have an impact on the developing hypothalamus, leading to abnormalities in appetite control and feeding. These hormones may also be involved in neural growth and development directly.
Abstract
Obesity in adults and children is increasingly becoming a major health problem worldwide. However, the precise biological mechanisms governing this disease have not been fully elucidated. Obesity involves the complex interaction of a wide range of environmental and genetic factors. Additionally, there is now a growing body of evidence suggesting that alterations in metabolic environment during important periods of organ development can predispose individuals to later development of obesity and diabetes. Maternal obesity or malnutrition during pregnancy increases the risk for metabolic disorders (including obesity) in the offspring. Similarly, early postnatal overnutrition also predisposes offspring to adult obesity. The hypothalamus appears to play an essential role in controlling appetite. It undergoes a tremendous growth beginning early in gestation and continuing during the postnatal period. These developmental windows represent periods of sensitivity for hypothalamic development during which alterations in the nutritional and/or hormonal environment may perturb hypothalamic development and subsequent function.