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No alcohol in January: benefits

The University of Sussex research showed that:

  • 93% of participants had a sense of achievement;
  • 88% saved money;
  • 82% think more deeply about their relationship with drink;
  • 80% feel more in control of their drinking;
  • 76% learned more about when and why they drink;
  • 71% realised they don’t need a drink to enjoy themselves;
  • 70% had generally improved health;
  • 71% slept better;
  • 67% had more energy;
  • 58% lost weight;
  • 57% had better concentration;
  • 54% had better skin.

Dr Richard de Visser’s findings come from three self-completed online surveys: 2,821 on registering for Dry January; 1,715 in the first week of February; and 816 participants in August.

A new YouGov poll undertaken for Alcohol Change UK showed that one in ten people who drink – an estimated 4.2 million people in the UK – are already planning to do Dry January in 2019.

Short-chain fatty acid fermentation products of the gut microbiome and the brain

Short-chain fatty acid fermentation products of the gut microbiome: implications in autism spectrum disorders.

Abstract

Recent evidence suggests potential, but unproven, links between dietary, metabolic, infective, and gastrointestinal factors and the behavioral exacerbations and remissions of autism spectrum disorders (ASDs). Propionic acid (PPA) and its related short-chain fatty acids (SCFAs) are fermentation products of ASD-associated bacteria (Clostridia, Bacteriodetes, Desulfovibrio). SCFAs represent a group of compounds derived from the host microbiome that are plausibly linked to ASDs and can induce widespread effects on gut, brain, and behavior. Intraventricular administration of PPA and SCFAs in rats induces abnormal motor movements, repetitive interests, electrographic changes, cognitive deficits, perseveration, and impaired social interactions.

The brain tissue of PPA-treated rats shows a number of ASD-linked neurochemical changes, including innate neuroinflammation, increased oxidative stress, glutathione depletion, and altered phospholipid/acylcarnitine profiles. These directly or indirectly contribute to acquired mitochondrial dysfunction via impairment in carnitine-dependent pathways, consistent with findings in patients with ASDs.

Of note, common antibiotics may impair carnitine-dependent processes by altering gut flora favoring PPA-producing bacteria and by directly inhibiting carnitine transport across the gut. Human populations that are partial metabolizers of PPA are more common than previously thought. PPA has further bioactive effects on neurotransmitter systems, intracellular acidification/calcium release, fatty acid metabolism, gap junction gating, immune function, and alteration of gene expression that warrant further exploration.

These findings are consistent with the symptoms and proposed underlying mechanisms of ASDs and support the use of PPA infusions in rats as a valid animal model of the condition. Collectively, this offers further support that gut-derived factors, such as dietary or enteric bacterially produced SCFAs, may be plausible environmental agents that can trigger ASDs or ASD-related behaviors and deserve further exploration in basic science, agriculture, and clinical medicine.

Obesity, antibiotic use, gut microbes and brain function

Obese pregnant mice exhibit changes in social behavior, oxytocin cells, synaptic plasticity, and the microorganism composition of the microbiota, but Lactobacillus reuteri could reverse these changes []. Because gut flora imbalance can increase the permeability of the intestinal mucosa, the metabolic products of gut microorganisms and certain cytokines can enter the circulation system and cause damage to the CNS, resulting in a delay in the early neurological development in child patients. Christensen used metabolomics to identify a large number of bacteria-derived metabolites that might be associated with ASD-related behaviors [].

Adams found that the levels of SCFAs, which are very important for the development of neurological functions, in the stool samples of autistic children were lower than those of normal children []; similarly, the PPA levels were also reduced. The exposure of pregnant rats to PPA before giving birth impaired the social behavior of their newborn and adolescent rats []. Moreover, following PPA injection into the brain ventricles of adult rats, the rats exhibited a behavioral change similar to that of human ASD, and the injection also induced changes in ASD-related genes, including genes for neurotransmitters, nerve cell adhesion factors, and oxidative stress [].

The bacterial metabolites, 4-ethyl-phenylsulfate and 3-(3-hydroxy phenyl)-3-hydroxypropionic acid, can cause mice to develop ASD-like symptoms []. In addition, the serum lipopolysaccharide (LPS, cell wall components of gram-negative bacteria) levels are significantly higher in ASD patients than in normal subjects, and LPS has a clear association with social disorders []. Most children with ASD have a history of infection before age 2, and the frequency of their use of antibiotics is also significantly higher than that of normally developed children [].

Antibiotics destroy the physiological balance of the inherent gut flora, and the newly colonized microorganisms produce neurotoxins, thereby inducing chronic diarrhea and ASD. For example, an abnormal increase in Clostridia and Bacteroidetes in the gut can promote gastrointestinal symptoms and ASD behaviors []. Therefore, both the imbalance of gut flora and the entry of excessive amounts of bacterial metabolites into the brain through the circulation are associated with the onset of ASD.

Hypothyroidism and cancer

Clinical hypothyroidism is a pervasive deficit in thyroid hormone actions, leading to the alteration of calorigenesis and oxygen consumption throughout the body and organ-specific effects. Deficiency of T3 actions at the genomic level cause hormonal, biochemical, ion-transport, and mechanical changes in target tissues. T4 is the principal hormone produced by the thyroid gland and in circulation.

Monodeiodination of its outer ring in both the cytoplasm and nucleus of target tissues converts it to T3 by the function of three tissue-specific deiodinases []. The actions of T3 are mediated by its binding to one of three receptor isoforms (TRα1, TRβ1, and TRβ2), which in turn form dimers with another T3 receptor or with other nuclear receptors. Subsequent DNA binding with specific orientations occurs at the 5′ regulatory regions of thyroid hormone-responsive genes to either activate or repress transcription [].

Based on this genetic description, some clinical manifestations are understood at the molecular level, including short stature as a result of failure to stimulate the growth hormone gene in pituitary somatotrophs, decreased low-density lipoprotein (LDL) cholesterol clearance because of a deficit in the expression of the hepatic LDL receptor gene regulated by sterol regulatory element binding transcription factor 2 and impaired diastolic and systolic ventricular function resulting from decreased myocardial sarcoplasmic reticulum ATPase and α-myosin heavy chain expression.

T3 also regulates cellular uptake of glucose and amino acids, augments cardiomyocyte calcium-ATPase activity, and alters adenosine triphosphate generation by the mitochondria []. As novel therapies continue to be identified for the treatment of neuroendocrine malignancies, hypothyroidism may also result because of the interaction of thyroid hormone with G protein-coupled membrane receptors and the mitogen activated protein kinase pathways.

Diagnosis

Signs and Symptoms

Common clinical features associated with hypothyroidism are tiredness and fatigue, weight gain, dry skin, cold intolerance, constipation, muscle weakness, facial edema, hoarse voice, and poor memory (Table 4). These symptoms can be present in other diseases, including malignancy, and can be side effects of cancer therapies.

Associations between metabolic syndrome, serum thyrotropin, and thyroid antibodies status in postmenopausal women, and the role of interleukin-6.

Our study confirms that metabolic syndrome in both euthyroid and subclinical hypothyroid women is connected with obesity, visceral fat accumulation, and higher TSH and IL-6 concentrations. Immune thyroiditis is associated with higher TSH and IL-6 levels. Obese subclinical hypothyroid women with Hashimoto`s thyroditis have a higher prevalence of metabolic syndrome when compared with subclinical hypothyroid women without thyroid autoimmunity. It is possible that in the crosstalking between subclinical hypothyroidism and metabolic syndrome, enhanced proinflammatory cytokine release in the course of immunological thyroiditis plays a role.

https://www.ncbi.nlm.nih.gov/pubmed/26457493

Improved sanitation and mycotoxin eradication to prevent stunted growth

Despite improvements in crop production and poverty levels, the WHO estimates that 24% of children are stunted globally, totaling 171 million children. Stunting is a form of chronic malnutrition when children fall below their height-for-age median, leading to cognitive impairment and lifelong economic loss. Nutritional supplementation has failed to improve the prevalence of stunting, prompting alternative explanations that include environmental enteric dysfunction (EED), an inflammatory intestinal abnormality, and mycotoxin exposures. Both of these associated factors are climate-dependent.

A systematic review of primary research was conducted in PubMed and WHO databases following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A total of 191 studies were identified; 27 met the inclusion criteria, and 23 articles were selected and related to stunting, EED, and mycotoxins. Recently published clinical trials were unsuccessful at resolving EED with immunosuppressant, antiparasitic, or dietary therapies.

A stunting factor known to co-occur with EED is mycotoxin exposure from contaminated grains and groundnuts, although the pathway linking mycotoxin exposure to stunting is unclear. Current studies have evaluated influences of reducing exposure and removing mycotoxins from affected foods, although the results have been unclear. Research in EED and mycotoxicity is underway but remains elusive in mitigating childhood stunting. Climate change and environmental factors will further exacerbate both factors by increasing the difficulty of proper sanitation establishment and shortening the time food can be safely stored in humidity.

Efforts at reducing stunting, particularly among developing countries, need to focus on improved sanitation and mycotoxin eradication in the context of changing climates.

Positive effects of micronutrients delivered after 24 mo of age

A large body of evidence suggests that the first 1000 d from conception is a critical window in which interventions to address malnutrition will be most effective, but little is known about the impact on linear growth of nutritional interventions in children ≥2 y of age. The aim of this analysis was to evaluate the effectiveness of several nutrition-based interventions, specifically iron, zinc, calcium, iodine, vitamin A, multiple (≥2) micronutrients, protein, and food, at improving growth in children ≥2 y of age. A systematic search of MEDLINE and EMBASE retrieved 7794 articles.

A total of 69 studies met prespecified inclusion criteria. Baseline height-for-age z score, age, nutrient dose, and study duration were examined as potential sources of heterogeneity. Zinc (mean effect size: 0.15; 95% CI: 0.06, 0.24), vitamin A (0.05; 95% CI: 0.01, 0.09), multiple micronutrients (0.26; 95% CI: 0.13, 0.39), and protein (0.68; 95% CI: 0.30, 1.05) had significant positive effects on linear growth, with baseline height-for-age z score as a significant inverse predictor of the effect size. Iron, calcium, iodine, and food-based interventions had no significant effect on growth.

Age at baseline, study duration, and dose were not related to effect size for any nutrient examined. These findings suggest that zinc, vitamin A, multiple micronutrients, and protein interventions delivered after 24 mo of age can have a positive effect on linear growth, especially in populations that have experienced growth failure.

To eat or not to eat almonds

Evidence suggests that eating nuts may reduce the risk of cardiovascular disease (CVD). We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating almond consumption and risk factors for CVD. MEDLINE, Cochrane Central, Commonwealth Agricultural Bureau, and previous systematic reviews were searched from 1990 through June 2017 for RCTs of ≥3 wk duration that evaluated almond compared with no almond consumption in adults who were either healthy or at risk for CVD.

The most appropriate stratum was selected with an almond dose closer to 42.5 g, with a control most closely matched for macronutrient composition, energy intake, and similar intervention duration. The outcomes included risk factors for CVD. Random-effects model meta-analyses and subgroup meta-analyses were performed. Fifteen eligible trials analyzed a total of 534 subjects.

Almond intervention significantly decreased total cholesterol (summary net change: −10.69 mg/dL; 95% CI: −16.75, −4.63 mg/dL), LDL cholesterol (summary net change: −5.83 mg/dL; 95% CI: −9.91, −1.75 mg/dL); body weight (summary net change: −1.39 kg; 95% CI: −2.49, −0.30 kg), HDL cholesterol (summary net change: −1.26 mg/dL; 95% CI: −2.47, −0.05 mg/dL), and apolipoprotein B (apoB) (summary net change: −6.67 mg/dL; 95% CI: −12.63, −0.72 mg/dL). Triglycerides, systolic blood pressure, apolipoprotein A1, high-sensitivity C-reactive protein, and lipoprotein (a) showed no difference between almond and control in the main and subgroup analyses.

Fasting blood glucose, diastolic blood pressure, and body mass index significantly decreased with almond consumption of >42.5 g compared with ≤42.5 g. Almond consumption may reduce the risk of CVD by improving blood lipids and by decreasing body weight and apoB. Substantial heterogeneity in eligible studies regarding almond interventions and dosages precludes firmer conclusions.

How to Prevent Mold

The main things mold needs to grow in a home are organic materials to feed on and moisture. In houses there are always plenty of organic materials for mold to live on such as wood, drywall and various other building materials.

Moisture, on the other hand, can be controlled practically and so keeping the moisture in your home low is the best way to prevent mold growth.

Prevent Mold by Preventing Moisture

Most molds need 24-48 hours of moisture to begin to grow. Therefore if a suitable material in your home is wet for more than 24 hours then you run the risk of mold starting to grow.

Prevent Mold by Preventing Water Leaks

There are a few main things which usually cause moisture problems in the home. One is water leaks. These include things such as leaking roofs or walls, leaking pipes and leaking taps or a leaking shower.

If you know of any leaks in your home you should fix them without delay. You might need to inspect your home to find any water leaks you didn’t know about.

Prevent Mold by Preventing Condensation

Condensation is another frequent cause of moisture. Condensation forms on cold surfaces when water vapor in the air cools and becomes liquid. Often you’ll see condensation on metal pipes, concrete walls, water tanks and windows.

One way to reduce condensation is to keep the temperature warmer in rooms. For example, by installing insulation. You can also insulate the surfaces themselves such as putting coverings over metal pipes. You’ll also have less condensation occurring if you keep the humidity in your home low.

Prevent Mold by Reducing Humidity

Prevent Mold
Dehumidifier

Many species of mold can begin to grow from humidity alone if the humidity stays high for long enough. In fact the humidity only needs to be higher than 55% before some molds can begin to grow.

The best way to keep humidity low in your home is through ventilation. Open the windows during the day, especially when it’s hot since this is when humidity is usually the lowest outside. Close your windows when it’s raining outside though.

It’s especially important to ventilate the rooms where steam and moisture builds up, like the kitchen and bathroom. Exhaust fans help to reduce the humidity when doing things like cooking or washing dishes.

Air conditioners can also reduce household humidity, as can using dehumidifiers in your home.

Wet Clothes and Preventing Mold

One common cause of moisture problems in homes is wet clothes. After you’ve washed your clothes you should immediately dry them. Don’t leave them sitting in a wet pile for a long time. Make sure not to leave any wet clothes lying around waiting to be washed too.

It’s best to dry your clothes outside on a clothes line if you can. Hanging them inside on a clothes horse or indoor clothes line will not dry them as quickly and the moisture from your clothes will evaporate into the air, raising the humidity. If you dry them in a clothes dryer inside your home then you should exhaust the air outdoors if possible. In either case make sure the room where you’re drying your clothes is well ventilated.

Mold and Clothes

Removing Mold

Once mold has begun to grow in your home it’s not enough to just take away the mold’s moisture source. Mold that runs out of moisture can lie dormant for a long time without dying. So if you already have mold growth in your home you need to take steps to have it removed.

Killing Mold
Mold Removal and Remediation

Mold Food Sources and Cleaning to Prevent Mold

Mold grows and feeds on organic substances such as wood or cotton. Mold should not grow on surfaces like plastic, metal or glass unless there is a layer of grease or some other organic substance which it can feed on.

Some materials mold commonly grows on in the home include wood, carpet, food, paper, insulation, wallpaper, paint, wallpaper glue, plasterboard, fabrics, cotton, books, leather, chipboard, furniture, dust, ceiling tiles, inside air conditioners and almost any other organic material.

You should clean regularly to reduce dirt and grime which mold can live on. Dust and vacuum often, ideally with a HEPA (High Efficiency Particulate Air) filtered vacuum cleaner to remove dust and other substances that mold can grow off of. It has been found that 80% of mold grows on dust.

For more information about vacuum cleaners and mold visit Vacuum Mold.

Minimizing Mold Spores to Prevent Mold

Mold spores are everywhere in the air outside. They float through buildings all the time and there is no practical way to remove all mold spores indoors.

However if the concentration of mold spores inside is significantly higher than outside then it can start to cause health issues. A higher amount of mold spores also increases the potential for mold problems to start.

Mold spores enter homes through windows, doors, air ducts, etc. They can also be transported inside attached to skin, clothing, hair, pets, etc.

Although you cannot eliminate all mold spores inside your home or prevent all mold spores from entering, minimizing the amount of spores will prevent you from suffering mold related health problems and lessen the chance of mold beginning to grow in your home.

To minimize mold spores clean and dust often. Also vacuum your home regularly, preferably with a HEPA vacuum cleaner to remove mold spores. HEPA air filters in your home also help remove mold spores from the air.

Sunlight to Prevent Mold

Mold loves dark spaces indoors to grow in. Allowing sunlight in will reduce the chances of mold growing so open the curtains in rooms during the day to let natural light in.

Warmth and Preventing Mold

Mold generally does not grow in cold environments. Warm, humid conditions are ideal for mold growth. Most molds need temperature of 70 degrees Fahrenheit (20 degrees Celsius) or more to grow.

Weapons Against Cancer: Millions of Bacteria Programmed to Kill  

Genetically modified microbes release “nanobodies” that alert the immune system to cancer in mice, scientists report.

A scanning electron micrograph of immune cells, blue, attacking cancer cells. Tumors may elude the immune system, but researchers are harnessing reprogrammed bacteria to destroy cancer cells in mice.CreditSteve Gschmeissner/Science Source

CreditCreditSteve Gschmeissner/Science Source

Scientists have used genetically reprogrammed bacteria to destroy tumors in mice. The innovative method one day may lead to cancer therapies that treat the disease more precisely, without the side effects of conventional drugs.

The researchers already are scrambling to develop a commercial treatment, but success in mice does not guarantee that this strategy will work in people. Still, the new study, published on Wednesday in the journal Nature Medicine, is a harbinger of things to come, said Dr. Michael Dougan, an immunologist at Massachusetts General Hospital in Boston.

“At some point in the future, we will use programmable bacteria for treatment,” said Dr. Dougan, whose research laid some groundwork for the new study. “I think there’s just too much potential.”

Our immune cells can sometimes recognize and destroy cancer cells without assistance. But tumors may hide from the immune system by taking advantage of a gene called CD47.

 

Normally, the gene makes a protein that studs the surface of red blood cells, a kind of sign that reads, “Don’t Eat Me.” Immune cells see it, and pass by healthy red blood cells.

But as red blood cells age, they lose CD47 proteins. Eventually the immune cells no longer give them a free pass, gobbling up old cells to make way for new ones.

Mutations in cancer cells can cause them to switch on the CD47 gene. The immune system sees these cells, too, as harmless, allowing them to grow into dangerous tumors.

In recent years, scientists have been developing antibodies that can attach to CD47 proteins on cancer cells, masking the “Don’t Eat Me” sign. Then the body’s immune cells learn to recognize the cancer cells as dangerous and attack.

But standard antibodies are big molecules that can’t burrow into a large tumor. And since they have to be injected into the bloodstream, these antibodies end up everywhere in the body, causing side effects.

 

Nicholas Arpaia, an immunologist at Columbia University in New York, and Tal Danino, a synthetic biologist, wondered if they could use bacteria to turn the immune system against cancer cells — but from within tumors, rather than from outside.

Ordinary bacteria will colonize tumors in the body, using them as a refuge from the immune system. In 2016, Dr. Danino helped construct bacteria that can make drugs to fight tumors after entering them.

Bacteria cannot make normal antibodies for CD47. But recently, Dr. Dougan and his colleagues developed a tiny version of the molecule called a nanobody.

Not only are nanobodies small enough for bacteria to produce, they’re also much more potent than conventional antibodies.

The researchers inserted the nanobody gene into the bacteria, turning them into nanobody factories. Then the team injected five million of the altered microbes into mouse tumors.

The bacteria were also programmed to commit mass suicide. After they established themselves and multiplied, 90 percent of the bacteria ripped themselves apart, spilling out nanobodies. The nanobodies attached to CD47 proteins on the cancer cells, robbing them of their camouflage.

In addition, fragments of the dead bacteria leaked out of the tumor. These bits of debris drew the attention of immune cells, which attacked the uncloaked cancer cells.

Inside the besieged tumor, the surviving bacteria started multiplying again. When the population grew large enough, the majority committed suicide once more — delivering another pulse of nanobodies and fragments.

The double-whammy may eliminate the tumors into which the bacteria were injected.

When Dr. Dougan and his colleagues originally developed their CD47 nanobody, they recognized that transporting it to cancer cells would be crucial to its effectiveness. But he never imagined that someone would hide it inside a microbial Trojan Horse.

“I love it when this kind of thing happens,” he said. “It’s a great little machine.”

The approach also has the potential to reduce the side effects of cancer treatment. Rather than flooding the body of the mice with medicine, the bacteria coordinated targeted attacks on the tumors. And thanks to their small size, the nanobodies that leaked from the cancer cells were quickly cleared by the body.

Dr. Arpaia and his colleagues reported an additional benefit. After they killed off one tumor with bacteria, other tumors in the mice also shrank. It is possible that the bacteria helped the immune system learn to recognize other cancer cells.

Dr. Danino co-founded a company, GenCirq, that is exploring using these reprogrammed bacteria to treat cancer. Dr. Arpaia is on the leadership board.

Their goal is to treat some forms of metastatic cancer with a pill of programmed bacteria. In earlier research, Dr. Danino and colleagues showed that bacteria swallowed by mice can reach the liver and invade tumors there.

That’s significant, because the liver is often colonized by metastatic cancer. If genetically reprogrammed bacteria help the immune cells recognize a tumor there, they may be able to attack cancers elsewhere in the body.

 

Dr. Dougan cautioned that the genetically reprogrammed bacteria might not be as powerful in people as they seem to be in mice.

“We have basically the same plumbing, but just on a much larger scale,” he said. “What that means is that stuff doesn’t as efficiently move from one part of a person to another.”

The new study demonstrates how far the field of synthetic biology has come in recent years, said Tim Lu, a computational biologist at M.I.T. and a co-founder of a company, Synlogic, that is also reprogramming bacteria to fight cancer.

“These things are not just seen as crazy things to play with,” said Dr. Lu. “They potentially could actually make their way into patients.”

Carl Zimmer writes the “Matter” column. He is the author of thirteen books, including “She Has Her Mother’s Laugh: The Powers, Perversions, and Potential of Heredity.” @carlzimmer  Facebook

A version of this article appears in print on , on Page D3 of the New York edition with the headline: Bacteria, Altered to Destroy Cancer. Order Reprints | Today’s

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This is a diagram of the viral proteins

COAT OF PROTEINS MAKES VIRUSES MORE INFECTIOUS AND LINKS THEM TO ALZHEIMER’S DISEASE

Herpes simplex virus type 1 (HSV-1) and respiratory syncytial virus (RSV) interact with biological fluids, creating a coat of proteins around the viral surface. This results in the viruses becoming more infectious and can contribute to the formation of amyloid plaques. In animal models, researchers found these viruses can bind to amyloid proteins, which aggregate into plaques that contribute to Alzheimer’s disease. HSV-1 is able to accelerate the transformation of soluble amyloid proteins into amyloid plaques. READ MORE…

Reuse and do not reheat some foods

What you can do instead?

You can use the leftover chicken in salads or sandwich, or re-cook the chicken on the stove on a very low flame.

2. Potatoes

How many times have you just reheated this food?

One of the most commonly used food item, potatoes are often used in most households during several meals in a day, sometimes, all the meals. But this is not the best practice.

You shouldn’t reheat it because

It is rich starchy food that has many health benefits.

When reheated it promotes the growth of botulism a rare bacteria. However, it can’t be killed by reheating in microwave. It may instead lead to food-poisoning.

What can you do instead?

The best way is it to re-cook them in a shallow pan.

3. Spinach

Popeye’s favourite food is very nutritious but you must avoid reheating them.

You shouldn’t reheat it because:

It contains a lot of nitrates which convert to nitrites when reheated, and nitrites are carcinogenic in nature.

What can you do instead?

You can either eat it after steaming it or just cool it quickly and keep it below 5 degrees celsius to prevent nitrite production.

4. Oil

Many times you reheat the leftover cooking oil and prepare pakodas not realising that it can greatly harm your body.

You shouldn’t reheat it because

You should know that your cooking oil should be heated at a low flame, thereby, helping it release less smoke.

In case you reheat previously heated oil, it is likely to release toxic fumes and harmful free-radicals.

What can you do instead?

The best way would be to discard the oil and not re-use it.

5. Beetroot

You shouldn’t reheat it because:

Beetroots just like spinach are nitrate-rich foods.

Reheating them converts nitrates to nitrites which is carcinogenic to the body and can also give you a stomach ache.

What can you do instead?

If there’s any leftover rather than reheating it’s better to eat it cold.

6. Rice

Rice is the most common leftover item in our kitchen and also most commonly reheated food.

However, it’s best to avoid reheating it in a microwave.

You shouldn’t reheat it because

Uncooked rice contains spores of bacteria and reheating it does not kill this bacteria.

So, if the rice is left standing at room temperature, the spores automatically multiply.

This may prove to be toxic and cause vomiting and even diarrhea.

What can you do instead?

Boil water and add the leftover rice to it.

Don’t over-boil the rice as it would become soggy.

You’ll find that the rice would look and taste as good as new.

7. Eggs

This staple breakfast food also should not be reheated.

Best known as a protein powerhouse, reheating boiled or scrambled eggs should be avoided.

You shouldn’t reheat it because

The protein in eggs is destroyed once it’s exposed to heat over and over again.

Also they become toxic and unfit for consumption once they have been cooked.

What can you do instead?

You can chop the boiled eggs and use them in a green salad.