How Is Alzheimer’s Disease Diagnosed? Cognitive Testing, Blood Work and Brain Imaging

The grocery list is still on the counter. Not forgotten, exactly. Written, re-read, then written again on a second sheet with the same items in a slightly different order. Her daughter notices both lists on a Tuesday visit and says nothing, then lies awake that night wondering whether this is ordinary aging or the start of something with a name.

That uncertainty is where almost everyone begins, and it is why people search for how Alzheimer’s is diagnosed long before anyone in the family says the word out loud. The good news is that the process is more orderly than most people imagine. It does not hinge on one frightening scan or one failed quiz.

What follows is a plain account of what clinicians actually do, in what order, and what each step can and cannot tell you. Where the evidence is still unsettled, particularly around blood tests, this article says so.

How Alzheimer's is diagnosed: why there is no single test

Alzheimer’s disease is a condition in which abnormal proteins build up in the brain and nerve cells gradually lose their connections and die. The National Institute on Aging describes it as the most common cause of dementia in older adults, where dementia is the umbrella word for a decline in thinking severe enough to interfere with daily life.

Here is the first thing to understand about how Alzheimer’s is diagnosed: clinicians are answering two separate questions. The first is whether thinking has genuinely changed from what was normal for this person. The second is what is causing that change. Memory loss has many possible causes, and several of them are treatable, including thyroid problems, vitamin B12 deficiency, depression, medication side effects and untreated sleep apnea.

That is why the pathway is layered. A history and cognitive testing answer the first question. Blood work and a structural brain scan rule out the look-alikes. Only after that do specialized tests for Alzheimer’s proteins come into play, and even then, not for everyone.

For decades, Alzheimer’s could be confirmed with certainty only after death, by examining brain tissue. That has shifted. Spinal fluid analysis and amyloid PET imaging can now show the characteristic protein changes in a living person, and blood tests that detect the same signals are moving from research into clinical use. Still, no guideline treats any single result as a verdict. The diagnosis remains a clinical judgment built from converging evidence, which is slower than people want but considerably more reliable than any one number.

What actually happens at the first memory appointment

The first visit is usually with a primary care clinician, and it is mostly conversation. Expect to be asked when the changes started, whether they came on gradually or suddenly, and what specifically has become harder: paying bills, following a recipe, finding words, navigating a familiar route. Clinicians want examples, not labels.

A second voice matters enormously. The NHS and NIA both note that someone who knows the person well is often asked to describe what they have observed, because people with early memory problems may not notice or may minimize them. This is not an accusation. It is simply that the person living with the change is the least able to see it from the outside.

Then comes the review of everything else. A full medication list, including over-the-counter sleep aids and antihistamines, because several common medicines cloud thinking in older adults. Alcohol intake. Mood and sleep. Hearing and vision, since struggling to hear a conversation can look like struggling to follow one. A history of head injury, stroke, Parkinson’s disease or seizures.

The physical and neurological exam checks reflexes, balance, coordination, muscle tone, eye movements and sensation. Clinicians are looking for signs that point away from Alzheimer’s, such as the tremor and stiffness of Parkinson’s-related conditions or the one-sided weakness that suggests small strokes.

Finally, a brief screening test of memory and thinking is done in the room. If it raises concern, the clinician orders blood work, often a brain scan, and in many health systems a referral to a specialist memory service or neurologist. Walking out of that first visit without a diagnosis is normal and expected.

Alzheimer's diagnosis tests: what cognitive screening measures

Cognitive testing sounds intimidating. In practice, it is a set of short tasks that sample different thinking skills: repeating a list of words and recalling them a few minutes later, drawing a clock face set to a specific time, naming objects, counting backward, copying a shape, following a multi-step instruction.

The two most widely used screening tools are the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA). Both are scored out of 30 points, as the NHS notes in its description of dementia assessment. The MoCA is generally more sensitive to the subtle changes of early disease because it puts more weight on attention, planning and delayed recall.

What are clinicians actually reading in the results? Not just the total. The pattern matters. Alzheimer’s typically affects the ability to store new memories first, so a person may repeat the words back perfectly right away but recall none of them five minutes later, even with hints. Other causes of cognitive decline produce different fingerprints: trouble with attention and planning but intact memory suggests a vascular or frontal pattern, for example.

Scores are also interpreted against the individual. A retired professor and a person who left school at fourteen should not be held to the same cutoff, and reputable clinicians adjust for education, language and cultural background. The NIA notes that these screens are designed to flag concern, not to diagnose.

When screening is borderline or the picture is complicated, a referral for neuropsychological testing may follow. This is a longer evaluation, often two to three hours, conducted by a psychologist trained in brain-behavior relationships, and it maps strengths and weaknesses across many domains in far finer detail.

Blood work: ruling out the conditions that mimic Alzheimer's

Standard blood tests cannot confirm Alzheimer’s. Their job in the diagnostic pathway is the opposite: to find something else. The NHS lists this step as routine in any dementia assessment, and for good reason. A surprising number of people referred for memory concerns turn out to have a correctable problem.

Thyroid function is checked because an underactive thyroid slows thinking, mood and movement in ways that can look like dementia. Vitamin B12 and folate levels are measured because deficiency damages nerves and impairs memory, and because absorption of B12 declines with age and with some common stomach-acid medicines. A complete blood count looks for anemia, which starves the brain of oxygen and causes fatigue and fog. Kidney and liver function tests matter because waste products that these organs normally clear can accumulate and cause confusion. Blood glucose is checked because both high and low sugar disturb cognition. Electrolytes such as sodium are included because imbalances, often from dehydration or medications, are a frequent cause of acute confusion in older adults.

Depending on history, clinicians may add tests for syphilis, HIV or inflammatory markers, since each can affect the brain. None of these is accusatory; they are simply on the list of reversible causes that no one wants to miss.

Finding an abnormality does not automatically mean it explains everything. Someone can have both a low B12 level and early Alzheimer’s. What it does mean is that the treatable problem gets treated, and cognition is reassessed afterward before anyone draws conclusions. This step is where the phrase ‘rule out’ earns its keep, and it is one reason a careful diagnosis takes more than one appointment.

Brain scan for dementia: what MRI and CT show and what they miss

A structural brain scan, meaning an image of the brain’s physical shape, is part of most dementia evaluations. The two options are computed tomography (CT), which uses X-rays, and magnetic resonance imaging (MRI), which uses a magnetic field and radio waves and gives a sharper picture of soft tissue.

The first purpose is exclusion. Both scans can reveal a tumor, a bleed, a buildup of fluid pressing on the brain (hydrocephalus), or the scattered scars of past strokes. Any of these can produce memory and thinking changes, and each calls for a different conversation than Alzheimer’s does. Mayo Clinic describes imaging as a way to rule out these other explanations before attributing symptoms to Alzheimer’s.

The second purpose is pattern recognition. In Alzheimer’s, the hippocampus, a seahorse-shaped structure deep in each temporal lobe that is essential for forming new memories, tends to shrink early. MRI can show this shrinkage, along with a broader loss of volume in the temporal and parietal lobes. Radiologists compare what they see against what is expected for the person’s age.

What these scans cannot do is prove Alzheimer’s. Some shrinkage is normal with aging. Some people with clear Alzheimer’s symptoms have scans read as unremarkable, especially early. And other conditions, including frontotemporal dementia, shrink different regions, which helps with sorting but is not definitive on its own.

So a ‘normal’ MRI is reassuring about tumors and strokes, but it does not close the question. A scan showing hippocampal atrophy raises the probability of Alzheimer’s without settling it. Either way, the result is one piece set beside the history and the cognitive testing, never a standalone answer.

Amyloid and tau: PET scans and spinal fluid testing explained

Two proteins define Alzheimer’s at the microscopic level. Beta-amyloid clumps into plaques between nerve cells. Tau, a protein that normally stabilizes the internal scaffolding of neurons, becomes abnormally twisted and forms tangles inside them. For most of medical history, these could only be seen under a microscope after death.

Positron emission tomography (PET) changed that. A PET scan involves injecting a small amount of a radioactive tracer that binds to a specific target, then imaging where it accumulates. Amyloid PET tracers light up plaques; tau PET tracers, developed more recently, light up tangles. The NIA describes both as tools that can show these protein changes in living people. A separate type, FDG-PET, measures how the brain uses glucose and can reveal regions of reduced activity in a pattern typical of Alzheimer’s.

Cerebrospinal fluid analysis offers a different window on the same biology. Cerebrospinal fluid is the clear liquid that cushions the brain and spinal cord, collected through a lumbar puncture, where a thin needle is placed between the bones of the lower back under local anesthetic. The fluid is analyzed for amyloid and tau levels. In Alzheimer’s, amyloid in the fluid typically drops, because it is being trapped in plaques, while tau rises as neurons are damaged. The procedure sounds alarming to many people; in practice it is a routine outpatient test, though headache afterward is a known and usually temporary side effect.

Neither test is used in everyone. Guidelines reserve them for situations where the diagnosis is uncertain, where the person is younger than typical, where symptoms are unusual, or where confirming the presence of amyloid would change management. A positive amyloid result in someone with no symptoms does not equal a diagnosis of Alzheimer’s dementia, a distinction that matters more every year.

Blood test for Alzheimer's: where the evidence actually stands

The question people now ask most is whether a simple blood test can diagnose Alzheimer’s. The honest answer is: increasingly, in part, within limits.

Researchers have identified forms of tau and amyloid in blood plasma that track closely with what is found in spinal fluid and on PET scans. The NIA notes that such blood biomarker tests are being developed and, in some settings, used to help identify Alzheimer’s-related changes. The appeal is obvious. A blood draw is cheaper, faster and far less daunting than a lumbar puncture or a PET scan.

Several cautions belong alongside the enthusiasm. First, these tests have been studied largely in specialist clinics and research cohorts, which means their performance in a general primary care population, with its mix of other health conditions, is still being established. Second, kidney function, body weight and other factors can shift some biomarker levels, which complicates interpretation. Third, a positive result indicates the presence of Alzheimer’s-type brain changes, not that those changes are the cause of a person’s current symptoms. Many older adults have some amyloid buildup without dementia.

For these reasons, mainstream guidance treats blood biomarkers as a tool to be used by clinicians within a full evaluation, often to decide who needs confirmatory testing, rather than as a stand-alone screen for the worried well. Direct-to-consumer testing without a clinician to interpret the result and the context around it is not recommended by any of the major health bodies cited here.

Expect this picture to evolve. The science is moving quickly, and what is confirmatory today may be routine tomorrow. The underlying principle will not change: a biomarker tells you about biology, and a diagnosis tells you about a person.

Who is usually referred for full testing, and who is asked to wait

Not everyone who forgets a name needs a dementia work-up, and not everyone who worries about Alzheimer’s is headed for a PET scanner. Clinicians make a judgment about who moves forward and who is watched.

A full evaluation is generally pursued when memory or thinking changes are affecting daily function, when they are reported by both the person and someone close to them, when they have progressed over months, or when they appear alongside changes in personality, language or spatial judgment. Younger age at onset is another trigger for more thorough testing, because Alzheimer’s before the mid-sixties is less common and other explanations become relatively more likely. Mayo Clinic and the NIA both describe specialist referral as appropriate when the primary care picture is unclear.

Who is asked to wait, or more precisely to return for reassessment? Often it is the person whose screening test is normal and whose concerns are mainly about occasional word-finding lapses or misplaced objects, which the NIA describes as common in normal aging. It is also frequently the person whose blood work revealed a treatable issue; cognition is rechecked once that issue is addressed. And it is the person in the middle of an acute illness, a bereavement or a depressive episode, because each of these can temporarily impair thinking and the assessment is more reliable once things have settled.

Waiting is not dismissal. A documented baseline score today becomes the comparison point in six or twelve months, and change over time is one of the most informative signals a clinician has. If symptoms worsen in the meantime, the pathway reopens. People are entitled to say when they feel brushed off, and to ask for the reasoning behind a decision to watch rather than test.

How the tests compare: what each one can and cannot tell you

A single table clarifies more here than several paragraphs would. Each tool in the diagnostic pathway answers a specific question, and none answers all of them.

Test	What it involves	What it can show	Key limitation
History and informant interview	Structured conversation with the person and someone who knows them	Whether and how thinking has changed from baseline	Relies on memory and insight of those reporting
Cognitive screening (MMSE, MoCA)	Short pencil-and-paper or verbal tasks, scored out of 30	Pattern and degree of impairment across memory, attention, language	Flags concern; does not identify the cause
Neuropsychological testing	Extended assessment by a specialist psychologist	Detailed cognitive profile; distinguishes patterns	Lengthy; access varies
Routine blood work	Standard blood draw	Thyroid, B12, anemia, metabolic and infectious causes	Cannot confirm Alzheimer’s
MRI or CT	Structural brain imaging	Tumors, strokes, bleeds, fluid buildup, pattern of shrinkage	Shrinkage overlaps with normal aging
Amyloid or tau PET	Radioactive tracer plus imaging	Presence and location of Alzheimer’s proteins	Positive result does not equal dementia; limited availability
Spinal fluid analysis	Lumbar puncture	Amyloid and tau levels reflecting brain changes	Invasive; post-procedure headache possible
Blood biomarkers	Blood draw for plasma tau or amyloid	Likelihood of Alzheimer’s pathology	Still being validated outside specialist settings

Reading down the right-hand column makes the logic of the whole process visible. Every test has a blind spot, and the sequence is arranged so that each one covers the gap left by the one before. That is the real reason a diagnosis takes several steps rather than one.

The weeks after the first visit: what the timeline usually looks like

People often picture a diagnosis as a single conversation. In reality it unfolds across several appointments, and the NHS describes a pathway that begins with a general practitioner and, where appropriate, continues at a specialist memory service.

The first stretch is practical. Blood tests are drawn, usually within days, and results return within a week or two in most settings. If the clinician ordered a brain scan, scheduling depends on local availability and can range from days to several weeks. Many people find this interval the hardest part, because nothing visible is happening and the mind fills the silence.

Next comes the specialist assessment if one was arranged. Here the cognitive testing is repeated in more depth, the scan is reviewed, and the full picture is assembled. Some memory services complete this in a single long visit; others spread it over two or three. Where neuropsychological testing or biomarker tests are added, the timeline extends again.

The results conversation itself deserves preparation. Clinicians typically explain what was found, what diagnosis best fits, and how confident they are. It is reasonable to ask for that confidence level directly. It is also reasonable to bring a second person, to request a written summary, and to ask for a follow-up appointment to absorb and return with questions.

After a diagnosis of Alzheimer’s or mild cognitive impairment, the following weeks usually include a discussion of treatment options, which the prescribing clinician leads and which this article does not pre-empt. They also include referrals to support services, a review of driving and safety, and conversations about planning ahead while the person can take a full part in decisions about their own life. That last point is where many families later say they wished they had started sooner.

Mild cognitive impairment versus Alzheimer's: what the labels mean

One result that confuses many families is a diagnosis of mild cognitive impairment, often shortened to MCI. Mild cognitive impairment means measurable decline in memory or thinking that is greater than expected for age but not severe enough to disrupt independence in daily activities. A person with MCI may struggle to recall recent conversations yet still manage finances, cooking and medication without help.

MCI is a description of a stage, not a cause. It can be due to early Alzheimer’s, to vascular changes, to depression, to medication effects, or to something that never progresses at all. The NIA notes that an estimated 10 to 20 percent of people aged 65 or older with MCI develop dementia over a one-year period, which also means most do not progress in any given year, and some return to normal cognition.

Clinicians subdivide MCI by which skills are affected. Amnestic MCI, where memory is the main problem, is the form most often linked to later Alzheimer’s. Non-amnestic MCI, affecting attention, language or spatial ability more than memory, raises the possibility of other conditions. Biomarker testing is sometimes offered at this stage precisely because knowing whether amyloid is present reshapes the conversation about what MCI likely represents for this particular person.

Alzheimer’s dementia, by contrast, is diagnosed when cognitive decline has progressed to the point of interfering with daily function and the overall picture, supported by testing and imaging, fits Alzheimer’s rather than another cause. The line between the two is a clinical judgment about independence, not a fixed test score, and reasonable clinicians can place the same person slightly differently. What matters is that the label comes with a plan: regular reassessment, attention to reversible contributors, and a clear point of contact if things change.

What people often get wrong about Alzheimer's diagnosis

Myths cluster around this topic, and some of them cause real harm by delaying evaluation or inflating fear. A few deserve direct correction.

‘If I can still do the crossword, it is not Alzheimer’s.’ Preserved skills in one area say little about others. Early Alzheimer’s often spares long-practiced abilities, vocabulary and social grace while quietly eroding the storage of new memories. That is why clinicians test several domains rather than taking comfort from one.

‘Forgetting names means dementia is coming.’ The NIA is explicit that occasionally forgetting names or appointments and remembering them later is part of normal aging. The concern is a change in pattern: forgetting whole events rather than details, or being unable to retrieve the information even with cues.

‘A normal brain scan rules it out.’ As described above, MRI and CT exclude other causes and may show shrinkage, but a clean scan does not exclude Alzheimer’s, particularly early.

‘A positive amyloid test means I have dementia.’ Amyloid can accumulate for years before any symptoms, and some people with amyloid never develop dementia in their lifetime. The result describes biology, not destiny.

‘There is no point getting diagnosed because nothing can be done.’ An accurate diagnosis identifies the reversible causes that can be treated, opens access to support and planning, allows the person to make decisions while they can, and lets the treating team discuss whatever management options are appropriate for that individual.

‘Only old people get it.’ Alzheimer’s is strongly linked with age, but it does occur in people in their forties and fifties, and younger onset is a reason for more thorough testing, not less.

Each of these misunderstandings tends to push people toward either dismissing a real change or dreading an imaginary one. Evidence-based diagnosis exists to replace both with something more useful: an accurate picture.

Questions to ask your care team during the diagnostic process

A good diagnostic conversation is two-way. People who arrive with questions written down tend to leave with clearer answers and fewer regrets about what they forgot to ask. These are the ones clinicians are generally glad to be asked.

• What do my test results show, and how confident are you in this diagnosis right now?
• Have reversible causes such as thyroid, B12, medication effects, mood and sleep been fully checked and addressed?
• Which type of dementia do you think this is, and what makes you lean toward Alzheimer’s rather than another cause?
• Would further testing such as spinal fluid analysis, PET imaging or a blood biomarker test change what we do next? If not, why is it being suggested, or why not?
• Is this mild cognitive impairment or dementia, and what would make you change that assessment over time?
• How often should cognition be reassessed, and who coordinates that?
• What symptoms or changes should prompt us to contact you before the next scheduled appointment?
• Are there any of my current medicines that could be worsening my thinking?
• What support services, including for the person helping me, can you connect us with?
• Should we be discussing driving, work, finances or legal planning now, and who can help with that?
• If treatment is being considered, what is it intended to do, what are the known risks, and what is the realistic timeline for seeing any effect?

The last question is deliberately open. Decisions about whether any medication is appropriate, which one, and how it is started belong to the prescribing clinician in conversation with the person and their family. A trustworthy care team will welcome being asked to explain their reasoning, will say when something is uncertain, and will not rush a decision that can be made at the next visit with everyone better informed.

When to call your doctor: red-flag signs that should not wait

Most memory concerns can wait for a scheduled appointment. Some cannot. The distinction usually comes down to speed of onset and the presence of other symptoms.

Contact a clinician the same day, or seek emergency care, if confusion develops suddenly over hours or a day or two, especially in someone who was thinking clearly beforehand. Rapid onset points toward delirium, an acute disturbance of attention and awareness that is often caused by infection, dehydration, medication changes or another medical problem, and it needs prompt treatment. Seek urgent care if confusion comes with fever, severe headache, a stiff neck, new weakness or numbness on one side, slurred speech, facial drooping, vision loss, a seizure, or a recent fall or head injury. Any of these can signal stroke, bleeding or infection affecting the brain.

Call your doctor promptly, within days, if someone with known cognitive impairment shows a marked step-down in function, stops eating or drinking, becomes unusually drowsy, or develops new hallucinations or agitation. These may reflect a treatable intercurrent illness rather than disease progression.

Arrange a routine appointment if memory or thinking changes are gradual but persistent over months, if they are noticed by others, if they are starting to affect bills, medications, cooking or driving, or if there are changes in personality, judgment or language alongside the memory problems. The NIA and NHS both describe these as reasons to seek assessment rather than to wait and see.

Do not stop, start or change any prescribed medicine because of memory concerns without speaking to the prescriber first. If you suspect a medication is contributing, say so; that is a conversation the treating team wants to have, and it is theirs to resolve.

Frequently asked questions

Can a blood test for Alzheimer's replace a brain scan?

Not yet in routine practice. Blood tests measuring forms of tau and amyloid correlate well with spinal fluid and PET findings in research and specialist settings, and the NIA describes them as an emerging tool. Current guidance uses them within a full clinical evaluation, often to decide who needs confirmatory testing, rather than as a stand-alone diagnosis. A structural scan still has a separate job: excluding tumors, strokes and other causes.

What are the early signs that lead to an Alzheimer's diagnosis?

The most common trigger is repeatedly forgetting recently learned information, such as conversations or appointments, that cannot be recalled even with hints. Other early patterns include difficulty managing finances or following multi-step tasks, getting lost on familiar routes, trouble finding words, and changes in judgment or mood. The NIA distinguishes these from normal aging, where names or details are forgotten occasionally and remembered later.

How long does it take to get an Alzheimer's diagnosis?

It typically takes more than one appointment. The NHS describes a pathway that begins with a primary care assessment, followed by blood tests, often a brain scan, and referral to a specialist memory service when needed. Each step depends on local scheduling, so the total time varies widely between health systems and individuals. Clinicians also sometimes reassess after several months to see whether changes progress, which is informative rather than a delay.

Does a brain scan for dementia show Alzheimer's?

A standard MRI or CT does not prove Alzheimer’s. It rules out other causes such as tumors, bleeds, strokes and fluid buildup, and it may reveal shrinkage of the hippocampus and surrounding regions in a pattern consistent with Alzheimer’s. Specialized PET scans using tracers that bind amyloid or tau can show the actual protein changes, but these are reserved for specific situations and interpreted alongside the full clinical picture.

How does dementia affect attention span?

Attention is often affected, though the timing differs by cause. In Alzheimer’s, memory storage usually declines first, and difficulty sustaining focus, filtering distractions or shifting between tasks tends to become more noticeable as the disease progresses. In vascular dementia and Lewy body dementia, attention problems can appear early and may fluctuate from hour to hour. Cognitive tests such as the MoCA include attention tasks specifically to help clinicians distinguish these patterns.

Can a person with dementia live alone?

Some people with mild cognitive impairment or early dementia live alone safely for a period, particularly with support such as medication organizers, regular check-ins and simplified routines. The decision depends on the individual’s ability to manage safety, nutrition, medications and emergencies, not on the diagnosis alone. Clinicians and occupational therapists can assess this formally. Warning signs include missed medications, unexplained weight loss, unpaid bills, unsafe cooking incidents or getting lost.

What are some tips for caring for someone with Alzheimer's disease?

Keep routines predictable, reduce background noise during conversations, and offer simple choices rather than open questions. Use calendars, labels and written reminders placed where they will be seen. Approach from the front, make eye contact and speak in short sentences. Focus on feelings rather than correcting facts when confusion arises. The NIA and NHS both emphasize that caregivers also need rest, information and support, and that asking the care team about local services is part of good care.

How do you help a dementia patient sleep at night?

Start with daylight and activity: morning outdoor light, regular daytime movement and limiting naps help reset the body clock. Keep a consistent bedtime, dim lights in the evening, reduce caffeine after midday and keep screens out of the bedroom. Treat pain, bladder problems and sleep apnea, which commonly disrupt sleep. Because many sleep medicines worsen confusion in older adults, any medication question belongs with the treating clinician rather than the pharmacy shelf.

What is the difference between mild cognitive impairment and Alzheimer's?

Mild cognitive impairment describes measurable decline in memory or thinking that does not yet interfere with independence in daily activities. Alzheimer’s dementia is diagnosed when decline has progressed to affect daily function and the overall picture fits Alzheimer’s rather than another cause. MCI can have many causes and does not always progress; the NIA estimates 10 to 20 percent of people aged 65 and older with MCI develop dementia over a year.

Who should be present at a memory assessment?

Ideally the person being assessed and someone who knows them well, such as a spouse, adult child or close friend. The NHS and NIA both note that an informant’s account of day-to-day changes is a core part of the evaluation, because early memory problems are often invisible to the person experiencing them. A second person also helps remember what was said, which matters when the conversation covers results and next steps.

References

• National Institute on Aging (NIH): How Is Alzheimer's Disease Diagnosed?
• NHS: Alzheimer's disease, Diagnosis
• MedlinePlus: Alzheimer's Disease
• Cleveland Clinic: Alzheimer's Disease

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.