How Long Can a Person With Dementia Live Without Food?

How Long Can A Person With Dementia Live Without Food

Many people with dementia in its final stages might not eat or drink. Additionally, they could get dysphagia, which would make it difficult for them to swallow effectively. The amount of time a person can survive without food and water varies, but experts think adequate end-of-life care may help them live better.

Why do individuals with advanced dementia stop consuming food and liquids?

There are numerous causes for why someone can quit eating and drinking. Most people have a decline in activity and calorie requirements when a neurocognitive condition worsens.

The National Foundation of Swallowing Disorders estimates that at least 45% of patients with dementia also have dysphagia (or trouble swallowing) [1]. As a result, a person may be unable to consume enough nutrition and liquids.
Additionally, people with dementia might not maintain their oral hygiene as consistently as they once did. It can lead to sore mouths, infected teeth, and uncomfortable dentures [2].

Another possibility is that the brain damage has extended to the hypothalamus, which controls food intake [3]. Alternatively, it is possible that the person has lost the ability to recognize food or has stopped remembering to eat.

Aging can also be a factor in swallowing problems since the muscles lose bulk and become weaker and less mobile with age. The individual may feel as though they are choking on food or are unable to get it out of their mouth.

How long can a person with dementia survive without food or liquids?

Nobody knows how long someone can live without eating or drinking because it involves many variables. These factors include the person’s age, general health, and the ability of their immune system to combat infections.

Dysphagia is typically present in the later stages of neurocognitive disorders, so if someone has it, it may be a sign that their condition is worsening. As a result, there is a higher chance that someone will inhale food or fluids and develop a chest infection [4].

Although it is impossible to anticipate how long a person can go without eating or drinking, dysphagia can signal the beginning of end-of-life care [5].

What is artificial nutrition and hydration (ANH)?

Artificial nutrition and hydration (ANH) is a process in which medical professionals use a tube to administer nutrients and fluids intravenously into a patient’s body. This tube enters the stomach via the nose or a stomach-mounted device.

However, these doctors must provide such therapies in a healthcare facility, which many patients with neurocognitive disorders find stressful. Some people may attempt to take the tubes out.

Since it is unknown whether ANH offers any overall benefits, doctors do not usually advise this treatment for patients with late-stage dementia.

According to the American Speech-Language-Hearing Association, tube feeding does not enhance a dementia patient’s quality of life [6]. Furthermore, it claims that feeding through a tube does not lower their risk of getting a chest infection.

The Alzheimer’s Association advises people with neurocognitive disorders to plan their end-of-life care while they can still communicate and make decisions. It can include whether or not they desire ANH [7].

What indicators tell that an individual is nearing death?

When a person with dementia is on the verge of passing away, their condition worsens more quickly. They can become agitated and incontinent.

The Alzheimer’s Society of the UK lists the following as symptoms that a person with dementia is nearing death [8]:

  • loss of consciousness
  • unsteady breathing
  • restlessness
  • rattly sound in the chest
  • cold hands and feet

According to a 2019 study, pneumonia was the cause of mortality for 50% of those who needed hospital treatment because they had dementia [9].

Tips to support a person with late stage dementia

Doctors advise assisting patients to eat and drink for as long as possible, even if in small amounts. Here are some tips to help you support your late stage dementia patient.

  • Offer soft food.
  • Thicken liquids with unflavored gelatin or cornstarch.
  • Alternate bites of food with sips of fluid.
  • Offer ice cream or sherbet.
  • Serve finger food if the patient has trouble using cutlery.
  • Help the patient sit in an upright and comfortable position.


  1. Caregiver’s Guide to Dysphagia in Dementia. NFOSD. Published Online: 7th Feb, 2017. Accessed: 4th July, 2023.
  2. Espinosa-Val, M.C., Martín-Martínez, A., Graupera, M., Arias, O., Elvira, A., Cabré, M., Palomera, E., Bolívar-Prados, M., Clavé, P. and Ortega, O., 2020. Prevalence, risk factors, and complications of oropharyngeal dysphagia in older patients with dementia. Nutrients, 12(3), p.863.
  3. Vercruysse, P., Vieau, D., Blum, D., Petersén, Å. and Dupuis, L., 2018. Hypothalamic alterations in neurodegenerative diseases and their relation to abnormal energy metabolism. Frontiers in molecular neuroscience, 11, p.2
  4. Espinosa-Val, M.C., Martín-Martínez, A., Graupera, M., Arias, O., Elvira, A., Cabré, M., Palomera, E., Bolívar-Prados, M., Clavé, P. and Ortega, O., 2020. Prevalence, risk factors, and complications of oropharyngeal dysphagia in older patients with dementia. Nutrients, 12(3), p.863.
  5. End-of-Life Care for People With Dementia. National Institute on Aging. Accessed: 4th July, 2023.
  6. Alternative Nutrition and Hydration in Dysphagia Care. ASHA. Accessed: 4th July, 2023.
  7. End-of-life Planning. Alzheimer’s Association. Accessed: 4th July, 2023.
  8. How to know when a person with dementia is nearing the end of their life. Alzheimer’s Society. Accessed: 4th July, 2023.
  9. Manabe, T., Fujikura, Y., Mizukami, K., Akatsu, H. and Kudo, K., 2019. Pneumonia-associated death in patients with dementia: A systematic review and meta-analysis. PloS one, 14(3), p.e0213825.
  10. Dementia: How long can a person live without eating or drinking? Medical News Today. Published Online: 8th Aug, 2022. Accessed: 4th July, 2023.

Excessive Alcohol Consumption Accelerates Alzheimer’s Progression.

Excessive Alcohol Consumption Accelerates Alzheimer’s Progression

Researchers at Scripps Research and the University of Bologna have recently discovered that the combination of genetic predisposition and alcohol use disorder (AUD) may hasten the progression of Alzheimer’s. The study’s findings elucidate the molecular processes driving memory loss and may have broader ramifications for comprehending and managing Alzheimer’s, irrespective of the consumption of alcohol.

According to a recent study published in eNeuro, mice exposed to periodic high amounts of alcohol showed signs of cognitive loss about two months earlier than they would have otherwise. Ethanol increases the onset of Alzheimer’s disease (AD) by several months or possibly a few years in people with a hereditary predisposition to the disorder.

While there hasn’t been much research on how alcohol affects Alzheimer’s progression, epidemiological studies have indicated that alcohol use disorder may raise the overall risk of dementia development.

The researchers performed an experiment where mice were subjected to recurrent alcohol use over months, simulating the amounts of alcohol exposure reported in people with alcohol use disorder.

They contrasted the behavior of control mice with those with three particular gene mutations linked to an increased risk of Alzheimer’s.

What is the link between dementia & alcohol?

Previous studies have suggested a link between alcohol consumption and brain damage. The National Institute for Health and Care Excellence (NICE) and Alzheimer’s Disease International examined several research studies on the relationship between alcohol use and dementia development.

Both reviews adopted a systematic methodology in which experts assessed the findings of numerous earlier published research investigations.

These studies observed that people who drank heavily or binge drank (consuming a lot of alcohol quickly) had a higher risk of developing Alzheimer’s disease or any other form of dementia than people who drank moderately.

The NICE-evaluated research concentrated on sizable populations of hundreds or even thousands of people, commencing in mid-life (age 40–64). They followed them for more than five years, often far into old age, to examine how long-term behavioral habits could affect dementia risk.

How might alcohol harm the brain?

Brain damage can result from heavy alcohol use over an extended period. Long-term heavy drinkers are more likely to have less white matter in their brains, which aids in signal transmission between various brain regions. It may cause problems with how the brain works.

Additionally, prolonged heavy drinking can lead to thiamine B1 deficiency and Korsakoff’s syndrome, a memory condition that affects short-term memory.

How alcohol and genetic predisposition can accelerate Alzheimer’s onset?

The current study’s findings showed that mice exposed to alcohol gradually lost the ability to acquire and retain spatial patterns, and they started to exhibit these cognitive deficits earlier than mice in the control group.

The researchers discovered cognitive deficits in mice who received alcohol treatment almost two months before the standard period when such abnormalities would appear.

They thoroughly investigated the gene expression in the brains of those mice exposed to alcohol and those that weren’t to comprehend the underlying causes of alcohol use disorder.

They also compared the gene expression profiles of over 100,000 individual cells.

According to the findings, alcohol exposure caused significant changes in gene expression across the prefrontal brain.

The researchers observed increased expression of genes linked to neuronal excitability, neurodegeneration, and inflammation, specifically in the alcohol-exposed animals.

Supporting cells, including astrocytes, microglia, and endothelial cells, also showed abnormal gene expression patterns in reaction to alcohol exposure, indicating that these modifications were not confined to neurons.

Previously, neurons were primarily considered responsible for Alzheimer’s-related responses. Scientists have only recently discovered the involvement of these additional cell types in Alzheimer’s progression.

Alcohol alters gene expression, which may result in memory loss.

The researchers contrasted the gene transcription profiles of alcohol-exposed mice with the control group at different ages and stages of Alzheimer’s but with identical genetic backgrounds.

They found that the alcohol-exposed mice’s gene transcription profiles resembled older mice with more severe cognitive deterioration than mice their age.

Upon comparing the alcohol-exposed mice to the same type of mice at different Alzheimer’s stages (including mice without any impairments and severely compromised mice), the researchers found that alcohol exposure changed the gene expression patterns in a way typically associated with advanced stages.

How can it help in future research?

The first step toward understanding the molecular mechanisms underlying memory loss and creating treatments is to comprehend how gene expression changes in various cell groups throughout Alzheimer’s.

The researchers hypothesize that the gene transcription mechanisms involved in Alzheimer’s development with alcohol use disorder (AUD) may also contribute to the explanation of disease progression without alcohol use.

Although the researchers focused on familial Alzheimer’s in this study, the team plans to investigate whether alcohol usage also affects the incidence and course of sporadic Alzheimer’s in individuals who are not genetically prone to the disease in the future.


  1. Sanna, P.P., Cabrelle, C., Kawamura, T., Mercatelli, D., O’Connor, N., Roberts, A.J., Repunte-Canonigo, V. and Giorgi, F.M., 2023. A history of repeated alcohol intoxication promotes cognitive impairment and gene expression signatures of disease progression in the 3xTg mouse model of Alzheimer’s disease. Eneuro.
  2. National Institute for Health and Care Excellence, 2015. Dementia, disability and frailty in later life—mid-life approaches to delay or prevent onset. NICE guideline [NG16].
  3. Prince, M., Albanese, E., Guerchet, M. and Prina, M., 2014. World Alzheimer Report 2014. Dementia and Risk Reduction: An analysis of protective and modifiable risk factors (Doctoral dissertation, Alzheimer’s Disease International).
  4. Excess alcohol consumption may speed up progression of Alzheimer’s disease. Medical News Daily. Published Online: 23rd June, 2023. Accessed: 3rd July, 2023.
  5. Alcohol and Dementia. Alzheimer’s Society. Accessed: 3rd July, 2023.
  6. Alcohol in Excess Hastens Alzheimer’s Progression. Neuroscience. Published Online: 12th June, 2023. Accessed: 3rd July, 2023.

Scientists Discover How Too Much Sugar Intake May Raise Alzheimer’s Risk

Sugar Intake May Raise Alzheimer’s Risk

The precise biological mechanisms underlying this association between high blood sugar levels and an elevated risk of Alzheimer’s were previously unknown. A recent investigation into ATP-sensitive potassium (KATP) channels, which control cellular activity based on energy levels, has now clarified the relationship. It opens the door for potential novel therapies focused on particular channels as a fresh approach to treating the condition.

Although it is well known that patients with type 2 diabetes have a higher chance of getting Alzheimer’s, the precise explanation for this is still unclear and is the subject of ongoing research.

Recent research from Wake Forest University School of Medicine published in JCI Insight has revealed a novel mechanism that raises the risk of Alzheimer’s. According to the study, elevated blood glucose levels and higher sugar consumption are sufficient to produce amyloid plaque formation in the brain.

The study gives significant insights into the metabolic abnormalities linked with diabetes that make the brain vulnerable to Alzheimer’s.

Sugar linked to the development of toxic Alzheimer’s plaques

The study concentrated on a particular class of channels known as ATP-sensitive potassium (KATP) channels, which are crucial in controlling cell activity according to energy levels. The neuronal circuitry of the brain has a significant expression of KATP channels.

The researchers used a mouse model to show that consuming sugar water rather than regular drinking water increases the production of amyloid plaques.

Additionally, they found that higher blood sugar levels influence the brain’s beta-amyloid synthesis.

These results support the hypothesis that blood glucose levels and sugar consumption directly impact amyloid plaque generation, a significant hallmark of Alzheimer’s.

What are the cellular mechanisms underlying sugar’s influence on the brain?

The research team discovered a class of metabolic sensors termed ATP-sensitive potassium channels, or KATP channels, found in neurons while examining the underlying mechanisms. These pathways link changes in metabolism, neuronal activity, and beta-amyloid synthesis in the brain.

These KATP channels serve as energy regulators by monitoring the availability of ATP. ATP (Adenosine Triphosphate) is a vital energy source for cellular survival.

Disrupting the normal function of these sensors can disturb the brain’s regular functions and have consequences on its general functionality.

The researchers observed the expression of these metabolic sensors in Alzheimer’s patient’s brains. They again noticed changes in the presence of these channels.

According to the principal investigator, Dr. Shannon Macauley, they eliminated these sensors from the brain of mice using genetic procedures, demonstrating that a rise in blood sugar did not lead to an increase in beta-amyloid levels or amyloid plaques. The expression of these channels varies with an Alzheimer’s diagnosis, which again suggests that these metabolic sensors may contribute to the development of Alzheimer’s, as they discovered when they investigated the expression of these metabolic sensors in post-mortem human brains from Alzheimer’s patients.

What possible effects might this have on people who have Alzheimer’s?

This study emphasizes the critical role of KATP channels in the relationship between hyperglycemia and the risk of Alzheimer’s.

Dr. Macauley points out that the study not only provides one theory for why people with type 2 diabetes have an elevated chance of developing Alzheimer’s but also identifies a potential therapeutic target for curing the condition.

According to Dr. Merill, a geriatric psychiatrist and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center in Santa Monica, CA, treatments aimed at clearing up the mess of plaques left behind after the synapses and neurons have already died and gone may be less effective than early detection and correction of underlying drivers of Alzheimer’s, such as an inadequate elevation of blood sugar levels and the associated insulin resistance.

In theory, by targeting the KATP channels, the medications could lessen the influence of hyperglycemia on the formation of beta-amyloid, which is directly associated with the risk of developing Alzheimer’s.


  1. Grizzanti, J., Moritz, W.R., Pait, M.C., Stanley, M., Kaye, S.D., Carroll, C.M., Constantino, N.J., Deitelzweig, L.J., Snipes, J.A., Kellar, D. and Caesar, E.E., 2023. K ATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer’s disease–related pathology. JCI insight, 8(10).
  2. Cross, P.I., Could sugar consumption impact the risk of Alzheimer’s disease? Medical News Today. Published Online: 30th May, 2023. Accessed: 23rd June, 2023.
  3. Scientists discover that metabolic sensor may play role in Alzheimer’s disease. Medical Xpress. Published Online: 22nd May, 2023. Accessed: 23rd June, 2023.
  4. Sweet Trouble: How Sugar Intake Might Increase Alzheimer’s Risk. Published Online: 22nd May, 2023. Accessed: 23rd June, 2023.