Decreased semen and diet-Don't make the mistake of letting a diet kill sperm - UChicago Medicine

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Decreased semen and diet

Here are some things that can negatively impact your sperm count and sperm quality. Int J Androl. This article has been cited by other articles in PMC. Spermatozoa were classified as: immotile, motile without progression and motile with progressive movement. In: Male reproductive toxicology. Other studies Decerased inconclusive. Schlegel, a urologist at Weill Cornell Medicine, told CNN in an email that Decreased semen and diet new study "helps to solidify that dietary patterns in the father affect sperm production and quality. Open in qnd separate window.

Butch padilla. Some prescription medications have been known to lower sperm count.

It will lower your copper levels and can lead to long-term copper deficiency and way too much iron. Overview Low sperm count means that the fluid semen you ejaculate during an orgasm contains fewer sperm than normal. I went to the vit store and got some of the above supplements and in two days all I can say is thanks! I jerked off every other day 20 minutes of edging and maintained Bmx topless similar diet and water intake to the best of my ability. The supplements in this post will help make this possible. Share on: Facebook Twitter. Significant increase in concentration, motility, vitality and morphology of sperm. As a result, you may experience low-volume ejaculate. Supplements that boost semen quantity and quality L-ARGININE Simply put, L-Arginine is an amino acid that can be manufactured in the laboratory or synthesized by the body and sourced from different types Decreased semen and diet foods such as dairy products, poultry, red meat, nuts, and fish. It gives me a confidence boost and also a alpha male feeling. No spontaneous pregnancy was occurred after 12 Decreased semen and diet Moslemi MK, Tavanbakhsh S. A problem with the second stage can reduce the force with which semen is expelled.

Semen quality is a measure of male fertility , a measure of the ability of sperm in semen to accomplish fertilization.

  • Just as age weakens your muscles and changes your eyesight, it can reduce both the strength and volume of your ejaculation.
  • Poor ejaculation or low semen volume has many causes — at least partly because ejaculation is actually several processes that all happen at about the same time; and each can be impacted by what you eat, hormone levels, your general health and other factors.
  • Many studies have focused on male infertility.

Obesity is rapidly becoming a worldwide epidemic that affects children and adults. Some studies have shown a relationship between obesity and infertility, but until now it remains controversial. Thus, the aim of the present study was to investigate the effect of high-fat diet-induced obesity on male reproductive parameters. In a first experiment, male Wistar rats were fed a high-fat diet HFD or standard chow SD for 15, 30 or 45 weeks, after which they were evaluated by adiposity index, serum leptin levels, reproductive organ weights and sperm counts.

Sexual hormones and sexual behavior were evaluated in these animals, as well as fertility after natural mating. Another group of rats was submitted to motility analysis and fertility evaluation after in utero insemination. After 15, 30 or 45 weeks, HFD-fed animals presented significant increases in obesity index and serum leptin levels. Reproductive organ weights and sperm counts in the testis and epididymis were similar between the two groups at all timepoints studied.

Sexual behavior was not altered by the diet regimen, and HFD fertility after natural mating was also similar to SD-fed animals. Intergroup testosterone levels were also comparable, but estradiol levels were increased in HFD rats. Furthermore, sperm quality was reduced in HFD animals as evidenced by their decreased percentage of sperm with progressive movement. This altered motility parameter was followed by a trend toward reduction in fertility potential after artificial in utero insemination.

The results reported herein showed that obesity can affect sperm quality, by reducing sperm motility, without affecting other sperm parameters. The low sperm quality caused a slight reduction in fertility potential, showing that obesity may lead to impairment in male fertility. Overweight and obesity constitute a health problem of increasing prevalence and present a major public health concern [ 1 , 2 ] that affects men and women, young and old [ 3 ].

These two statuses are often defined simply as a condition of abnormal or excessive fat accumulation in adipose tissue [ 4 ] arising from an imbalance between calories ingested versus calories expended [ 5 ]. The change in the average weight of the population is occurring quickly, and within a few generations the bell-curve of human-weight distribution has shifted toward greater weight [ 3 ].

Obesity is a risk factor for non-insulin-dependent diabetes, cardiovascular disease, osteoarthritis, some types of cancer, and certain reproductive and metabolic disorders [ 6 ].

It is also associated with disturbance in the hormonal milieu that can affect the reproductive system, which is clear in women who present reproductive disorders when obese [ 7 , 8 ].

However, in men this relationship is poorly characterized, due to the lower number of studies in the literature [ 2 , 9 ]. In recent years, some studies have associated the body mass index BMI with reproductive parameters in men, showing that increased BMI is related to poor semen quality [ 10 ], decreased sperm concentration [ 11 ], decreased normal-motile sperm cells and increased DNA fragmentation index [ 12 ].

On the other hand, some works showed little or no relation between obesity and sperm concentration [ 2 , 13 ], motility or morphology [ 2 ] in men, even when serum reproductive hormone levels are altered [ 2 , 13 ].

A small number of energy-balance genes are known to be essential for normal body regulation and a loss-of-function mutation in a single gene can lead to obesity in laboratory animals [ 14 ]. However, it does not explain obesity in the majority of the human population where no such genetic changes have been identified. If obesity were entirely genetic in causation, it would be difficult to explain the increased in prevalence of obesity over the last few decades. Contemporary diets are a major factor in the current obesogenic environment, and most human obesity could probably be assessed as being diet-induced [ 14 ].

Although genetic obesity models are useful for finding the role of endogenous neuropeptides in body weight control, the best parallels to human obesity are provided by the physiological model of diet-induced obesity DIO [ 14 , 15 ]. In diet-induced obese male mice decreases in sperm motility [ 16 , 17 ], fertilization rate [ 17 ] number of plugs and pregnancy rate [ 16 ], as well as increases in sperm DNA damage and sperm intracellular reactive oxygen species ROS have been reported [ 17 ].

In studies of rats made obese by cafeteria feeding, a diminished number of ejaculations was observed [ 19 ]. Thus, in the literature, few studies report the effects of obesity on male fertility and sperm quality and the results are altogether less clear.

Therefore the aim of this study was to determine the effect of high-fat diet-induced obesity on reproductive parameters in male rats. During the experiment, animals were allocated individually into polypropylene cages, with laboratory grade pine shavings as bedding.

Rat chow and filtered tap water were provided ad libitum. The dietary regimen was adapted from previous studies [ 20 , 21 ]. The study was divided into two steps. In the first experiment 1 , rats were given the high-fat diet HFD or standard diet SD for 15, 30 or 45 weeks. In the second step experiment 2 the animals were exposed to HFD or SD for a period of 15 weeks, long enough to increase adiposity index, which characterizes obesity.

In this part of the study rats were given a high-fat diet HFD or standard diet SD for 15, 30 or 45 weeks. Rats were weighed every week, and food consumption was monitored daily. Blood was collected from the ruptured cervical vessels for determination of leptin levels.

Adipose tissue was isolated and weighed from the epididymal, visceral and retroperitoneal pad. The right testis, epididymis, vas deferens, ventral prostate and seminal vesicle without the coagulating gland were removed and their weights absolute and relative to body weights were determined. Testis and epididymis were used for sperm counts. Homogenization-resistant testicular spermatids stage 19 of spermiogenesis in the testis were counted as described previously by Robb et al.

Briefly, the testis, decapsulated and weighed soon after collection, was homogenized in 5 mL of NaCl 0. After a fold dilution, one sample was transferred to Neubauer chambers 4 fields per animal , and late spermatids were counted. To calculate the daily sperm production DSP , the number of homogenization-resistant spermatids was divided by 6. The sperm transit time through the epididymis was determined by dividing the number of sperm in each portion by the DSP. In this part of the study, animals were exposed to the high-fat or standard diet for 15 weeks, a period sufficient to characterize obesity.

Blood was collected from the ruptured cervical vessels for determination of sexual hormone levels testosterone, follicle stimulating hormone - FSH, luteinizing hormone - LH, estradiol. Three fat deposits - epididymal, visceral and retroperitoneal - were removed and weighed, as already described.

Semen was collected from the right and left deferens ducts to evaluate sperm motility and sperm morphology, respectively. The right testes were collected for in vitro testosterone assay. All samples were dosed in the same assay to avoid inter-assay errors. The intra-assay error was 3. The animals were observed in the dark period of the cycle in a separate room under dim red light, and all sexual behavior tests were performed h after the beginning of the dark period.

For the next 40 min the following parameters were evaluated: latency to the first mount, intromission and ejaculation; number of intromissions until the first ejaculation; latency of the first post ejaculatory intromission; number of post ejaculatory intromissions; and number of ejaculations [ 25 , 26 ].

The males that did not mount in the initial 10 min were considered sexually inactive. After the sexual behavior test the couples were kept together for an additional 4 hours. The animals that had been deemed inactive were tested one more time, for fertility, with different females in estrus. At the end of the afternoon males and females were separated and vaginal smears were collected.

The day on which sperm were found in the smear was determined to be gestational day 0 GD0 ; females were killed 20 days later to evaluate fertility. Immediately after euthanasia, the right vas deferens was collected. Sperm were obtained with the aid of a syringe and needle, through internal rinsing with 1. Sperm motility evaluation was performed by the same person throughout the study and was assessed by visual estimation spermatozoa per animal, in duplicate under a phase-contrast microscope Leica DMLS at X magnification.

Spermatozoa were classified as: immotile, motile without progression and motile with progressive movement. Sperm were also removed from the left vas deferens by internal rinsing with 1. Morphological abnormalities were classified into two general categories pertaining to head morphology without curvature, without characteristic curvature, pin head or isolated form, i.

Each piece was weighed and placed into a 1. The M was buffered with 0. After centrifugation 5 min, Because rats produce and ejaculate an excess of qualitatively normal sperm, artificial in utero insemination of a fixed critical number of sperm has been suggested as a means of increasing the sensitivity of a toxicant-induced decrease in sperm quality in the rat [ 30 ].

According to this technique, a fixed number of sperm collected from the cauda epididymis is inseminated directly into the uterus allowing evaluation of sperm quality, without the interference of other factors such as alterations of the sexual behavior pattern and number of sperm available for ejaculation [ 31 ].

Shortly after the room lights were turned off on the day of proestrus, the synchronized females were paired with sexually experienced, vasectomized males of proven sterility for 1 h. Receptive females that exhibited lordosis were selected for insemination. The isolation and preparation of proximal cauda sperm for insemination were the same as described previously [ 32 , 33 ], with the following adaptations.

One female was inseminated per male. All inseminations were performed while the recipient female was in a surgical plane using a mix of ketamine and xylazine anesthesia. The bifurcation of the uterine horns was exposed through a low, midventral incision. Fine curved forceps were used to elevate each horn while the insemination volume was injected through the wall of each horn via an gauge i.

Each injection site was cauterized immediately upon withdrawal of the needle. When insemination was completed, the abdominal musculature was sutured.

Females were killed 20 days later to evaluate fertility. On the GD20 the females that had been naturally and artificial inseminated were killed by decapitation.

After collection of the uterus and ovaries the numbers of corpora lutea, implants, reabsorptions and live and dead fetuses were determined. Two-way ANOVA for independent groups followed by the post hoc Tukey test were performed for comparison of results among the experimental groups in experiment 1. For experiment 2 Student t test or nonparametric Mann-Whitney test were used according to the characteristics of each variable. Throughout the course of the study, the mean food intake of HFD rats was significantly lower than the mean food intake of SD rats, in all experimental periods.

The capital letters refer to comparison between times, while lower case letters refer to the comparison between SD and HFD groups. When animals were compared in relation to time, the number of mature spermatids in the testis was lower in 30 and weeks animals in both experimental groups. As occurred in experiment 1, HFD rats showed a statically significant increase in adiposity index, body weight and weights of fat deposits data not shown after 15 weeks of diet exposure.

Sperm motility. Values expressed by median. Mann-Whitney test. Fertility parameters after natural mating and in utero artificial insemination of rats fed SD or HFD during 15 weeks. It is believed that with the increasing prevalence of sedentary lifestyles and dietary changes, obesity is emerging, in turn, as an important cause of adverse health outcomes, including male infertility [ 34 ].

Data from different population studies show an inverse relationship between BMI body mass index and fertility [ 10 , 11 ], although the mechanism by which fertility is affected is still unclear [ 35 ]. In an attempt to achieve deeper knowledge about obesity, several animal models have been developed, among which rodent models of diet-induced obesity DIO may provide the best parallels in relation to human obesity [ 14 , 15 , 18 ].

In this study, an obesity model induced by high-fat diet consumption was chosen.

Or it may be a sign of a problem with male hormone production. Sperm production or function can be affected by overexposure to certain environmental elements, including:. It is more than we saw back when we dated in the early 90s. Administering selenium plus N-acetyl-cysteine resulted in further beneficial effects in semen parameters They reported

Decreased semen and diet

Decreased semen and diet

Decreased semen and diet

Decreased semen and diet

Decreased semen and diet

Decreased semen and diet. related stories

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Diet-induced obesity in rats leads to a decrease in sperm motility

A study that analyzed sperm samples from nearly 43, men from around the world over a few decades found that sperm counts have dropped by more than half over the last 40 years. Although the definitive cause is unknown and additional research is needed to find the cause of the drastic decline in sperm counts , researchers have identified some habits and health conditions that may cause a decrease in sperm production. Here are some things that can negatively impact your sperm count and sperm quality.

The Cleveland Clinic notes that 5-alpha-reductase inhibitors used to treat prostate enlargement and hair loss such as finasteride, dutasteride, and propecia, can reduce one's volume of semen and number of sperm within their semen.

In some cases, this drop in semen production is temporary or reversible. Selective serotonin reuptake inhibitors, or SSRIs, used to treat depression and anxiety may also harm sperm or prevent it from moving through the reproductive tract.

Chemotherapy drugs will inhibit sperm production and other medications such as spironolactone, cimetidine, nifedipine, sulfasalazine, colchicine, and oral ketoconazole can also negatively impact male fertility. If you are on medication but concerned about your sperm count, do not discontinue taking your prescription medications or make any drastic lifestyle changes without first speaking to a healthcare professional. It's not only the medication taken to treat anxiety and depression that may be tied to a lowered sperm count.

A study published in the journal Neuroendocrinology Letters found that depression and anxiety in males has been linked to a decrease in semen volume and sperm density. According to Your Fertility, sexually transmitted infections like chlamydia, gonorrhea, syphilis, and mycoplasma genitalium can cause infertility if they are left untreated. Many STIs have few to no symptoms, which means they can oftentimes be left untreated for long periods of time. The earlier you have them diagnosed and treated, the less likely they are to impact your fertility.

In addition, low sperm count can be related to certain underlying medical conditions. A ccording to WebMD, those with an undescended testicle could face issues with lower sperm count and quality when a corrective surgery is not performed at an early age, which is typically before 18 months of age. Read More: 8 things you should never do right after having sex.

Environmental toxins, such as pesticides and heavy metals, can negatively affect sperm count. A study in the journal Current Urology Reports suggests that exposure to environmental toxins can impact semen quality , sperm concentration, motility, and morphology.

Several studies have been conducted to test the effects of mobile phone radiation on sperm count. A study in the Central European Journal of Urology found that men who kept their cell phones in their front pocket had a statistically lower number of sperm and a higher number of sperm cells with DNA fragmentation than those who did not keep their phones in their front pocket.

Read More: 6 scary things your phone can do to your mind and body. According to Trak Fertility, one of the common risk factors linked to low sperm count is the overheating of the testicles. The use of hot tubs, in particular, is not recommended for a man trying to conceive. A study by the University of California San Francisco found that exposures to hot tubs and hot baths can negatively impact male fertility — although the impact can be reversed.

In addition, there are mixed opinions on whether wearing tight underwear significantly contributes to elevated scrotal temperatures. Drugs, alcohol, and tobacco consumption have long been linked to serious health problems, including issues related to sperm motility and quality. The Cleveland Clinic warns that THC, the active ingredient in marijuana, decreases sperm production, affects sperm motility , and interferes with the production of testosterone.

Opiates can disrupt testosterone production and decrease the quantity and quality of the sperm. In addition, drinkers of 14 or more alcoholic beverages per week may have a decrease in testosterone production and an increase in estrogen production, which can lower sperm count.

In terms of smoking, a Brazilian study published in the journal BJU International comparing the sperm of smokers versus that of nonsmokers, found that smokers had a higher percentage of DNA fragmentation in their sperm samples. A study of 1, men published in the Journal Andrologia found that obesity was related to lower sperm count and lower sperm motility. Obesity also was found to increase the likelihood of physical defects in the sperm, including thin and pyriform pear-shaped heads.

Read More: 7 signs you're not overweight or obese, even if your BMI says you are. Vitamin deficiencies can negatively impact your overall health, but there are some vitamins that are important for fertility, especially vitamin D. A study published in the journal Human Reproduction found that men with a vitamin D deficiency had lower sperm counts and sperm motility than men with healthy vitamin D levels.

Read More: 10 subtle signs and symptoms of a vitamin D deficiency. There are some surgeries that can unintentionally impact your sperm count or sperm mobility.

For example, i nfertility is a recognized potential complication of inguinal hernia surgery , according to a review published in the Annals of Surgery. A study , presented at the European Society of Human Reproduction and Embryology's June conference, looked at the diets of 2, young Danish men to figure out how what they ate affected their sperm counts. The measure is an important factor in fertility, and also plays a role in sex drive and sexual function problems like erectile dysfunction.

The researchers categorized the men, who all took military fitness exams between and , by the type of foods they consumed regularly, or their "diet patterns. The researchers found that men who followed the prudent diet pattern had the highest sperm counts , while men who had a Western diet pattern had the lowest.

Men with vegetarian patterns had the second highest sperm counts, followed by men who ate in the more traditionally Danish way. For a June study, researchers at Aarhus University asked men about their bedtimes over a month's time. They found that men who went to sleep before p. The men with earlier bedtimes were four times as likely to have sperm count levels defined as "normal. It's possible that later bedtimes can weaken a person's immune system, causing it to overreact and attack sperm, lowering a man's overall count.

Sports injuries, car crashes, falls, and other accidents can cause testicular injuries. Larry Lipshultz of the Baylor College of Medicine explained that testicular trauma such as a testicular rupture, fracture, contusion, torsion, dislocation, or degloving of the scrotum can lead to male infertility , especially if not treated immediately. Julia Naftulin contributed to this reporting. Yvette Manes. Snapchat icon A ghost. Some prescription medications have been known to lower sperm count.

Lowered sperm count has been linked to depression and anxiety. Low sperm count can be caused by certain medical conditions or infections.

Exposure to toxins may affect sperm quantity. Overexposure to radiation may affect sperm production. Elevated scrotal temperatures can affect testicular function. Drugs, alcohol, and tobacco can decrease sperm quantity. Obesity can impact sperm production. A vitamin D deficiency can impact your sperm count. Low sperm count may be a result of prior surgical procedures. Eating junk food like pizza and chips could also lower your sperm count.

Your late-night Netflix habit could negatively affect your sperm count. Low sperm count can be caused by testicular trauma. Evergreen story Fertility.

Decreased semen and diet