According to social media, carbs come in various guises: naked carbs, net carbs, complex carbs and more.

You might be wondering what these terms mean or if all carbs are really the same. If you are into “carb counting” or “cutting carbs”, it’s important to make informed decisions about what you eat.

What are carbs?

Carbohydrates, or “carbs” for short, are one of the main sources of energy we need for brain function, muscle movement, digestion and pretty much everything our bodies do.

There are two classifications of carbs, simple and complex. Simple carbs have one or two sugar molecules, while complex carbs are three or more sugar molecules joined together. For example, table sugar is a simple carb, but starch in potatoes is a complex carb.

All carbs need to be broken down into individual molecules by our digestive enzymes to be absorbed. Digestion of complex carbs is a much slower process than simple carbs, leading to a more gradual blood sugar increase.

Fibre is also considered a complex carb, but it has a structure our body is not capable of digesting. This means we don’t absorb it, but it helps with the movement of our stool and prevents constipation. Our good gut bacteria also love fibre as they can digest it and use it for energy – important for a healthy gut.

What about ‘naked carbs’?

“Naked carbs” is a popular term usually used to refer to foods that are mostly simple carbs, without fibre or accompanying protein or fat. White bread, sugary drinks, jams, sweets, white rice, white flour, crackers and fruit juice are examples of these foods. Ultra-processed foods, where the grains are stripped of their outer layers (including fibre and most nutrients) leaving “refined carbs”, also fall into this category.

One of the problems with naked carbs or refined carbs is they digest and absorb quickly, causing an immediate rise in blood sugar. This is followed by a rapid spike in insulin (a hormone that signals cells to remove sugar from blood) and then a drop in blood sugar. This can lead to hunger and cravings – a vicious cycle that only gets worse with eating more of the same foods.

What about ‘net carbs’?

This is another popular term tossed around in dieting discussions. Net carbs refer to the part of the carb food that we actually absorb.

Again, fibre is not easily digestible. And some carb-rich foods contain sugar alcohols, such as sweeteners (like xylitol and sorbitol) that have limited absorption and little to no effect on blood sugar. Deducting the value of fibre and sugar alcohols from the total carbohydrate content of a food gives what’s considered its net carb value.

For example, canned pear in juice has around 12.3g of “total carbohydrates” per 100g, including 1.7g carb + 1.7g fibre + 1.9g sugar alcohol. So its net carb is 12.3g – 1.7g – 1.9g = 8.7g. This means 8.7g of the 12.3g total carbs impacts blood sugar.

The nutrition labels on packaged foods in Australia and New Zealand usually list fibre separately to carbohydrates, so the net carbs have already been calculated. This is not the case in other countries, where “total carbohydrates” are listed.

Does it matter though?

Whether or not you should care about net or naked carbs depends on your dietary preferences, health goals, food accessibility and overall nutritional needs. Generally speaking, we should try to limit our consumption of simple and refined carbs.

The latest World Health Organization guidelines recommend our carbohydrate intake should ideally come primarily from whole grains, vegetables, fruits and pulses, which are rich in complex carbs and fibre. This can have significant health benefits (to regulate hunger, improve cholesterol or help with weight management) and reduce the risk of conditions such as heart disease, obesity and colon cancer.

In moderation, naked carbs aren’t necessarily bad. But pairing them with fats, protein or fibre can slow down the digestion and absorption of sugar. This can help to stabilise blood sugar levels, prevent spikes and crashes and support personal weight management goals. If you’re managing diabetes or insulin resistance, paying attention to the composition of your meals, and the quality of your carbohydrate sources is essential.

A ketogenic (high fat, low carb) diet typically restricts carb intake to between 20 and 50g each day. But this carb amount refers to net carbs – so it is possible to eat more carbs from high-fibre sources.

Some tips to try

Some simple strategies can help you get the most out of your carb intake:

• reduce your intake of naked carbs and foods high in sugar and white flour, such as white bread, table sugar, honey, lollies, maple syrup, jam, and fruit juice

• opt for protein- and fibre-rich carbs. These include oats, sweet potatoes, nuts, avocados, beans, whole grains and broccoli

• if you are eating naked carbs, dress them up with some protein, fat and fibre. For example, top white bread with a nut butter rather than jam

• if you are trying to reduce the carb content in your diet, be wary of any symptoms of low blood glucose, including headaches, nausea, and dizziness

• working with a health-care professional such as an accredited practising dietitian or your GP can help develop an individualised diet plan that meets your specific needs and goals.

Correction: this article has been updated to indicate how carbohydrates are listed on food nutrition labels in Australia and New Zealand.

Saman Khalesi, Senior Lecturer and Discipline Lead in Nutrition, School of Health, Medical and Applied Sciences, CQUniversity Australia; Anna Balzer, Lecturer, Medical Science School of Health, Medical and Applied Sciences, CQUniversity Australia; Charlotte Gupta, Postdoctoral research fellow, CQUniversity Australia; Chris Irwin, Senior Lecturer in Nutrition and Dietetics, School of Health Sciences & Social Work, Griffith University, and Grace Vincent, Senior Lecturer, Appleton Institute, CQUniversity Australia

This article is republished from The Conversation under a Creative Commons license. Read the original article.

An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.

The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.

The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

What’s CJD got to do with Alzehimer’s?

CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Human growth hormone used to come from donated organs

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.

An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

What are the latest findings about Alzheimer’s disease?

The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.

They considered other explanations for the findings but concluded donated hGH was the likely cause.

Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.

Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

When was this process used in Australia?

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.

The risk is very low – and you can’t ‘catch’ it like a virus

The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.

Steve Macfarlane, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, Monash University

This article is republished from The Conversation under a Creative Commons license. Read the original article.