Motherhealth Caregivers Bay Area In-Home Care Hollistic

Caffeine has become the hot-topic of the moment. Its addition to so many products makes it important to know how long caffeine sticks around in the body in order to prevent possible overdose.

Caffeine takes a certain amount of time to work through your system. One study some years ago showed that the half-life of caffeine in healthy adults is 5.7 hours (see source). This means if you consume 200mg of caffeine at mid-day, you would still have 100mg in you at around 5.45pm.

What factors can delay caffeine’s half life?

The same study mentioned above showed that people with compromised liver function had a significantly longer half-life (a 49-year-old woman having alcoholic hepatic disease had a serum half-life of 168 hours).

Others can have genetic factors influencing the gene responsible for caffeine metabolism. The gene CYP1A2 is needed by the liver break down up to 95% of the caffeine in the body. Other genes can influence how well this gene does its job (src).

Some people may lack the gene or the gene may be defective. In this case, caffeine stays in the body a long time, increases sensitivity to caffeine, and can even cause allergy-like symptoms.

A variation of the gene PDSS2 also affects speed of metabolism. Those with the variation need a lot less caffeine to feel the stimulant affects.

Another study looked at how grapefruit juice may slow down caffeine metabolism in the liver, but it only was a slight inhibitor and wasn’t enough to cause warning.

What is the safe limit of caffeine in the body?

With caffeine levels in beverages and food continuing to climb – many people are asking – what exactly is the safe limit?

While the average caffeine consumption is around 200mg per day, The Mayo Clinic recommends that people not exceed to 500-600mg per day. Consuming more than this can result in adverse overdose symtoms. This of course is affected by body weight, health, and individual sensitivity.

People can build up a tolerance to the effects of caffeine requiring larger doses to produce the same desired effect. If you are unsure of how much you can handle, it is best to start small and gradually increase your caffeine consumption as needed. Sometimes a caffeine detox is needed to reset caffeine tolerance back to safer/normal amounts.

Those who have built up a high caffeine tolerance can have severe caffeine withdrawal symptoms when detoxing, so it may be wise to quit caffeine gradually.

A lethal dose of caffeine (LD50) consumed orally is equivalent to 150 milligrams per kilogram of body weight, which is what we base our Death by Caffeine application on.

In conclusion, the half life of caffeine might be around 6 hours, but can be influenced by other factors. Caffeine is a drug and should be used with discretion as well as respected.

By Caffeine Informer Staff

Holistic care for a 96 male with Dementia and Diabetes

Dementia is considered Type 2 Diabetes. He is 96 yr old and still ambulatory, walking back in forth to the living room and his bedroom toilet.

He loves to eat every 2 hours and goes to the toilet after drinking more than a glass of liquid. I suggested the following care to his caregivers as we tag team to offer in home non medical caregiving services to him:

Massage his head, shoulder and legs to get him to relax. Allow him to watch his favorite old cowboy movies. And to indulge in ice cream but in small servings. Add healthy variation to his snacks of crackers, cottage cheese, avocado, soft boiled eggs, cooked carrots, soup, decaf coffee and other healthy snacks.

Allow him to participate in decision making but act like a mother, caregiver, nurse and family. Remind him where the toilet is and where to walk. Ask permission to change his diapers that he calls underwear. Allow space for him at night when he starts to be grouchy or screams.

Medication schedule:

Most of his meds are separated in the morning and evening with meals. Give the melatonin and calcium with magnesium powder at night, 1 hour before bedtime. Give the probiotic at noon and evening and digestive enzymes and activated charcoal in the morning.

Omega 3 or fish oil is best given at noon.

Always give citrus fruits in the morning and noon. Give his breakfast at 4 or 7 am when he wakes up as he needs to drink some liquid. Serve small portion as he has extra weight already.

1. Eat in a quiet and calm room with limited distractions so that your loved one can focus on eating.
2. Eat meals together which can increase the likelihood that your loved one will eat the healthy meal provided.
3. Pack in protein. Even if your loved one cannot chew meat well, try eggs, milk-based pudding, or even protein powder.
4. Cut food into small pieces to make eating easier if your loved one can no longer use utensils.
5. Puree vegetables and add them to a shake if your loved one will not eat vegetables on their own.
6. Strengthen the prefrontal cortex responsible for dietary self-restraint by avoiding alcohol, getting adequate sleep, and exercising.

Research Sheds Light on How the Body Regulates Fundamental Neuro Hormone

New research has revealed a previously unknown mechanism in the body which regulates a hormone that is crucial for motivation, stress responses and control of blood pressure, pain and appetite. The breakthrough could be used to design drugs to help fight health problems connected with these functions in the future.

Researchers at the University of Bristol and University College London found that lactate – essentially lactic acid – causes cells in the brain to release more noradrenaline (norepinephrine in US English), a hormone and neurotransmitter which is fundamental for brain function. Without it people can hardly wake up or focus on anything.

The main cells of the brain, with neurons in yellow and astrocytes in orange. Adapted from the University of Bristol press release.

Production of lactate can be triggered by muscle use, which reinforces the connection between exercise and positive mental wellbeing.

Lactate was first discovered in sour milk by Swedish chemist, Carl Wilhelm Scheele in 1780. It is produced naturally by the body, for example when muscles are at work. In the brain, it has always been regarded as an energy source which can be delivered to neurones as fuel to keep them working when brain activity increases.

This research, published today in Nature Communications, identifies a secondary function for lactate as a signal between brain cells. It implies that there is an as yet unknown receptor for lactate in the brain which must be present on noradrenaline cells to make them sensitive to lactate.

Professor Sergey Kasparov, from Bristol University’s School of Physiology and Pharmacology, said: “Our findings suggest that lactate has more than one incarnation – in addition to its role as an energy source, it is also a signal to neurones to release more noradrenaline.”

Dr Anja Teschemacher, also from the University of Bristol, added: “The next big task is to identify the receptor which mediates this effect because this will help to design drugs to block or stimulate this response. If we can regulate the release of noradrenaline – which is absolutely fundamental for brain function – then this could have important implications for the treatment of major health problems such as stress, blood pressure, pain and depression.”

Astrocytes, small non-neuronal star-shaped cells in the brain and spinal cord, are the principle source of brain lactate. The discovery that astrocytes communicate directly with neurones opens up a whole new area of pharmacology which has been little explored.

Notes about this neuroscience research

The research was funded by the British Heart Foundation (BHF), the Medical Research Council (MRC), The Wellcome Trust and the Biotechnology and Biological Sciences Research Council (BBSRC).

Contact: Philippa Walker – University of Bristol
Source: University of Bristol press release

Waste Product of Exercise Protects Neurons from Trauma Damage

Researchers led by EPFL have found how lactate, a waste product of glucose metabolism can protect neurons from damage following acute trauma such as stroke or spinal cord injury.

Stroke or spinal cord injury can cause nerve cells to receive excessive stimulation, which ultimately damages and even kills them. This process is known as excitotoxicity, and it is one of the reasons why time following such trauma is critical, while it also implicated in progressive neurodegenerative diseases, e.g. Alzheimer’s disease. A team of scientists led by EPFL has now discovered that lactate, which is produced in the brain and even muscles after intense exercise, can be used to protect neurons against excitotoxicity. The study is published in the Nature journal Scientific Reports.

Following acute trauma such as a stroke or spinal cord injury, a certain type of receptors go into overdrive and overwhelm the target neuron with a barrage of electrical signals. This causes a build-up of calcium ions inside the neuron, which triggers toxic biochemical pathways that ultimately damage or kill it.

The receptors that cause this are called NMDA receptors, and interact with the neurotransmitter glutamate. NMDA receptors are a major target in research and medicine, as they are implicated in a number of disorders, including epilepsy, schizophrenia, Parkinson’s and even Alzheimer’s.

A team of researchers led by Pierre Magistretti from EPFL and the King Abdullah University of Science and Technology, investigated the effects of glutamate on cultured neurons from the brains of mice. The scientists used a new, non-invasive imaging technique called Digital Holographic Microscopy that can visualize cells structure and dynamics with nanometer-level resolution.

Previous studies have suggested that, lactate could protect neurons against excitotoxicity. Lactate is produced in the brain and in muscles after intense exercise as a waste product of glucose metabolism. Nonetheless, how lactate protects neurons has eluded scientists until now.

The researchers tested the effects of glutamate on the mouse neurons with and without lactate. The results were revealing: glutamate killed 65% of the neurons, but when with lactate, that number dropped to 32%.

The researchers then aimed to determine how lactate protects neurons. By using different receptor blockers on the mouse neurons, they determined that lactate triggers the production of ATP, the cell’s energy molecule. In turn, the produced ATP binds and activates another type of receptor in the neuron, which turns on a complex cascade of defense mechanisms. As a result, the neuron can withstand the onslaught of signals from the NMDA receptor.

The breakthrough can advance our understanding of neuroprotection, which could lead to improved pharmacological ways to ameliorate the irreparable damage caused by stroke, spinal cord injury, and other trauma.

ABOUT THIS NEUROSCIENCE RESEARCH

Funding: This work involved a collaboration of EPFL’s Brain Mind Institute with the King Abdullah University of Science and Technology, and the University Hospital of Lausanne (CHUV). It was funded by the FNRS and the NCCR Synapsy.

Source: EPFL
Image Credit: The image is credited to Pascal Jourdain (EPFL).
Original Research: Full open access research for “L-Lactate protects neurons against excitotoxicity: implication of an ATP-mediated signaling cascade” by P. Jourdain, I. Allaman, K. Rothenfusser, H. Fiumelli, P. Marquet and P. J. Magistretti in Scientific Reports. Published online February 19 2016 doi:10.1038/srep2125019

Abstract

L-Lactate protects neurons against excitotoxicity: implication of an ATP-mediated signaling cascade

Converging experimental data indicate a neuroprotective action of L-Lactate. Using Digital Holographic Microscopy, we observe that transient application of glutamate (100 μM; 2 min) elicits a NMDA-dependent death in 65% of mouse cortical neurons in culture.

In the presence of L-Lactate (or Pyruvate), the percentage of neuronal death decreases to 32%. UK5099, a blocker of the Mitochondrial Pyruvate Carrier, fully prevents L-Lactate-mediated neuroprotection. In addition, L-Lactate-induced neuroprotection is not only inhibited by probenicid and carbenoxolone, two blockers of ATP channel pannexins, but also abolished by apyrase, an enzyme degrading ATP, suggesting that ATP produced by the Lactate/Pyruvate pathway is released to act on purinergic receptors in an autocrine/paracrine manner.

Finally, pharmacological approaches support the involvement of the P2Y receptors associated to the PI3-kinase pathway, leading to activation of KATP channels. This set of results indicates that L-Lactate acts as a signalling molecule for neuroprotection against excitotoxicity through coordinated cellular pathways involving ATP production, release and activation of a P2Y/KATP cascade.

“L-Lactate protects neurons against excitotoxicity: implication of an ATP-mediated signaling cascade” by P. Jourdain, I. Allaman, K. Rothenfusser, H. Fiumelli, P. Marquet and P. J. Magistretti in Scientific Reports. Published online February 19 2016 doi:10.1038/srep2125019