Wireless device radiation and health

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https://en.wikipedia.org/wiki/Wireless_device_radiation_and_health 

 

A man speaking on a mobile telephone

 

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Antennas

The antennas contained in mobile phones, including smartphones, emit radiofrequency (RF) radiation (non-ionizing "radio waves" such as microwaves); the parts of the head or body nearest to the antenna can absorb this energy and convert it to heat. Since at least the 1990s, scientists have researched whether the now-ubiquitous radiation associated with mobile phone antennas or cell phone towers is affecting human health. Mobile phone networks use various bands of RF radiation, some of which overlap with the microwave range. Other digital wireless systems, such as data communication networks, produce similar radiation.

In response to public concern, the World Health Organization established the International EMF (Electric and Magnetic Fields) Project in 1996 to assess the scientific evidence of possible health effects of EMF in the frequency range from 0 to 300 GHz. They have stated that although extensive research has been conducted into possible health effects of exposure to many parts of the frequency spectrum, all reviews conducted so far have indicated that, as long as exposures are below the limits recommended in the ICNIRP (1998) EMF guidelines, which cover the full frequency range from 0–300 GHz, such exposures do not produce any known adverse health effect. In 2011, International Agency for Research on Cancer (IARC), an agency of the World Health Organization, classified wireless radiation as Group 2B – possibly carcinogenic. That means that there "could be some risk" of carcinogenicity, so additional research into the long-term, heavy use of wireless devices needs to be conducted. The WHO states that "A large number of studies have been performed over the last two decades to assess whether mobile phones pose a potential health risk. To date, no adverse health effects have been established as being caused by mobile phone use."

International guidelines on exposure levels to microwave frequency EMFs such as ICNIRP limit the power levels of wireless devices and it is uncommon for wireless devices to exceed the guidelines. These guidelines only take into account thermal effects, as non-thermal effects have not been conclusively demonstrated. The official stance of the British Health Protection Agency (HPA) is that "[T]here is no consistent evidence to date that Wi-Fi and WLANs adversely affect the health of the general population", but also that "... it is a sensible precautionary approach ... to keep the situation under ongoing review ...". In a 2018 statement, the FDA said that "the current safety limits are set to include a 50-fold safety margin from observed effects of Radio-frequency energy exposure".

Exposure

Mobile phones

A mobile phone connects to the telephone network by radio waves exchanged with a local antenna and automated transceiver called a cellular base station (cell site or cell tower). The service area served by each provider is divided into small geographical areas called cells, and all the phones in a cell communicate with that cell's antenna. Both the phone and the tower have radio transmitters which communicate with each other. Since in a cellular network the same radio channels are reused every few cells, cellular networks use low power transmitters to avoid radio waves from one cell spilling over and interfering with a nearby cell using the same frequencies.

Mobile phones are limited to an effective isotropic radiated power (EIRP) output of 3 watts, and the network continuously adjusts the phone transmitter to the lowest power consistent with good signal quality, reducing it to as low as one milliwatt when near the cell tower. Tower channel transmitters usually have an EIRP power output of around 50 watts. Even when it is not being used, unless it is turned off, a mobile phone periodically emits radio signals on its control channel, to keep contact with its cell tower and for functions like handing off the phone to another tower if the user crosses into another cell. When the user is making a call, the phone transmits a signal on a second channel which carries the user's voice. Existing 2G, 3G, and 4G networks use frequencies in the UHF or low microwave bands, 600 MHz to 3.5 GHz. Many household wireless devices such as WiFi networks, garage door openers, and baby monitors use other frequencies in this same frequency range.

Radio waves decrease rapidly in intensity by the inverse square of distance as they spread out from a transmitting antenna. So the phone transmitter, which is held close to the user's face when talking, is a much greater source of human exposure than the tower transmitter, which is typically at least hundreds of metres away from the user. A user can reduce their exposure by using a headset and keeping the phone itself farther away from their body.

Next generation 5G cellular networks, which began deploying in 2019, use higher frequencies in or near the millimetre wave band, 24 to 52 GHz. Millimetre waves are absorbed by atmospheric gases so 5G networks will use smaller cells than previous cellular networks, about the size of a city block. Instead of a cell tower, each cell will use an array of multiple small antennas mounted on existing buildings and utility poles. In general, millimetre waves penetrate less deeply into biological tissue than microwaves, and are mainly absorbed within the first centimetres of the body surface.

Cordless phones

The HPA also says that due to the mobile phone's adaptive power ability, a DECT cordless phone's radiation could actually exceed the radiation of a mobile phone. The HPA explains that while the DECT cordless phone's radiation has an average output power of 10 mW, it is actually in the form of 100 bursts per second of 250 mW, a strength comparable to some mobile phones.

Wireless networking

Most wireless LAN equipment is designed to work within predefined standards. Wireless access points are also often close to people, but the drop off in power over distance is fast, following the inverse-square law. However, wireless laptops are typically used close to people. WiFi had been anecdotally linked to electromagnetic hypersensitivity but research into electromagnetic hypersensitivity has found no systematic evidence supporting claims made by sufferers.

Users of wireless networking devices are typically exposed for much longer periods than for mobile phones and the strength of wireless devices is not significantly less. Whereas a Universal Mobile Telecommunications System (UMTS) phone can range from 21 dBm (125 mW) for Power Class 4 to 33 dBm (2W) for Power class 1, a wireless router can range from a typical 15 dBm (30 mW) strength to 27 dBm (500 mW) on the high end.

However, wireless routers are typically located significantly farther away from users' heads than a phone the user is handling, resulting in far less exposure overall. The Health Protection Agency (HPA) says that if a person spends one year in a location with a WiFi hot spot, they will receive the same dose of radio waves as if they had made a 20-minute call on a mobile phone.

The HPA's position is that "... radio frequency (RF) exposures from WiFi are likely to be lower than those from mobile phones." It also saw "... no reason why schools and others should not use WiFi equipment." In October 2007, the HPA launched a new "systematic" study into the effects of WiFi networks on behalf of the UK government, in order to calm fears that had appeared in the media in a recent period up to that time. Michael Clark of the HPA says published research on mobile phones and masts does not add up to an indictment of WiFi.

Effects studied

See also: Electromagnetic radiation and health

Blood–brain barrier

A 2010 review stated that "The balance of experimental evidence does not support an effect of 'non-thermal' radio frequency fields" on the permeability of the blood-brain barrier, but noted that research on low frequency effects and effects in humans was sparse. A 2012 study of low-frequency radiation on humans found "no evidence for acute effects of short-term mobile phone radiation on cerebral blood flow".

Cancer

See also: Non-ionizing radiation

There is no known way in which radiofrequency radiation (in contrast to ionizing radiation) affects DNA and causes cancer. In 2011 the IARC, a World Health Organization working group, classified mobile phone use as "possibly carcinogenic to humans". The IARC summed up their conclusion with: "The human epidemiological evidence was mixed. Several small early case–control studies were considered to be largely uninformative. A large cohort study showed no increase in risk of relevant tumours, but it lacked information on level of mobile-phone use and there were several potential sources of misclassification of exposure. The bulk of evidence came from reports of the INTERPHONE study, a very large international, multicentre case–control study and a separate large case–control study from Sweden on gliomas and meningiomas of the brain and acoustic neuromas. While affected by selection bias and information bias to varying degrees, these studies showed an association between glioma and acoustic neuroma and mobile-phone use; specifically in people with highest cumulative use of mobile phones, in people who had used mobile phones on the same side of the head as that on which their tumour developed, and in people whose tumour was in the temporal lobe of the brain (the area of the brain that is most exposed to RF radiation when a wireless phone is used at the ear)". The CDC states that no scientific evidence definitively answers whether mobile phone use causes cancer.

In a 2018 statement, the US Food and Drug Administration said that "the current safety limits are set to include a 50-fold safety margin from observed effects of radiofrequency energy exposure".

On 1 November 2018, the US National Toxicology Program published the final version (after peer review that was performed through March 2018) of its "eagerly anticipated" study using rats and mice, conducted over some ten years. This report concludes after the review with an updated statement that "there is clear evidence that male rats exposed to high levels of radio frequency radiation (RFR) like that used in 2G and 3G cell phones developed cancerous heart tumors.... There was also some evidence of tumors in the brain and adrenal gland of exposed male rats. For female rats, and male and female mice, the evidence was equivocal as to whether cancers observed were associated with exposure to RFR". An analysis of preliminary results from the study argued that due to such issues as the inconsistent appearances of "signals for harm" within and across species and the increased chances of false positives due to the multiplicity of tests, the positive results seen are more likely due to random chance. The full results of the study were released for peer review in February 2018.

A 2021 review concluded 5G radio frequencies in the range of 450 MHz to 6,000 MHz are probably carcinogenic for humans, particularly for gliomas and acoustic neuromas. Conclusions could not be drawn for higher frequencies due to insufficient adequate studies.

Fertility and reproduction

A decline in male sperm quality has been observed over several decades. Studies on the impact of mobile radiation on male fertility are conflicting, and the effects of the radio frequency electromagnetic radiation (RF-EMR) emitted by these devices on the reproductive systems are currently under active debate. A 2012 review concluded that "together, the results of these studies have shown that RF-EMR decreases sperm count and motility and increases oxidative stress". A 2017 study of 153 men that attended an academic fertility clinic in Boston, Massachusetts found that self-reported mobile phone use was not related to semen quality, and that carrying a mobile phone in the pants pocket was not related to semen quality.

A 2021 review concluded 5G radio frequencies in the range of 450 MHz to 6,000 MHz affect male fertility, possibly affect female fertility, and may have adverse effects on the development of embryos, foetuses and newborns. Conclusions could not be drawn for higher frequencies due to insufficient adequate studies.

Electromagnetic hypersensitivity

Main article: Electromagnetic hypersensitivity

Some users of mobile phones and similar devices have reported feeling various non-specific symptoms during and after use. Studies have failed to link any of these symptoms to electromagnetic exposure. In addition, EHS is not a recognized medical diagnosis.

Glucose metabolism

According to the National Cancer Institute, two small studies exploring whether and how mobile phone radiation affects brain glucose metabolism showed inconsistent results.

Effects on children

A report from the Australian Government's Radiation Protection and Nuclear Safety Agency (ARPANSA) in June 2017 noted that:

The 2010 WHO Research Agenda identified a lack of sufficient evidence relating to children and this is still the case. ... Given that no long-term prospective study has looked at this issue to date this research need remains a high priority. For cancer in particular only one completed case-control study involving four European countries has investigated mobile phone use among children or adolescents and risk of brain tumour; showing no association between the two (Aydin et al. 2011). ... Given this paucity of information regarding children using mobile phones and cancer ... more epidemiological studies are needed.

Base stations

Cellular mobile and UHF antenna tower with multiple antennas

Experts consulted by France considered it was mandatory that the main antenna axis should not to be directly in front of a living place at a distance shorter than 100 metres. This recommendation was modified in 2003 to say that antennas located within a 100-metre radius of primary schools or childcare facilities should be better integrated into the city scape and was not included in a 2005 expert report. The Agence française de sécurité sanitaire environnementale as of 2009, says that there is no demonstrated short-term effect of electromagnetic fields on health, but that there are open questions for long-term effects, and that it is easy to reduce exposure via technological improvements. A 2020 study in Environmental Research found that "Although direct causation of negative human health effects from RFR from cellular phone base stations has not been finalized, there is already enough medical and scientific evidence to warrant long-term liability concerns for companies deploying cellular phone towers" and thus recommended voluntary setbacks from schools and hospitals.

Safety standards and licensing

To protect the population living around base stations and users of mobile handsets, governments and regulatory bodies adopt safety standards, which translate to limits on exposure levels below a certain value. There are many proposed national and international standards, but that of the International Commission on Non-Ionizing Radiation Protection (ICNIRP) is the most respected one, and has been adopted so far by more than 80 countries. For radio stations, ICNIRP proposes two safety levels: one for occupational exposure, another one for the general population. Currently there are efforts underway to harmonize the different standards in existence.

Radio base licensing procedures have been established in the majority of urban spaces regulated either at municipal/county, provincial/state or national level. Mobile telephone service providers are, in many regions, required to obtain construction licenses, provide certification of antenna emission levels and assure compliance to ICNIRP standards and/or to other environmental legislation.

Many governmental bodies also require that competing telecommunication companies try to achieve sharing of towers so as to decrease environmental and cosmetic impact. This issue is an influential factor of rejection of installation of new antennas and towers in communities.

The safety standards in the US are set by the Federal Communications Commission (FCC). The FCC has based its standards primarily on those standards established by the National Council on Radiation Protection and Measurements (NCRP) a Congressionally chartered scientific organization located in the WDC area and the Institute of Electrical and Electronics Engineers (IEEE), specifically Subcommittee 4 of the "International Committee on Electromagnetic Safety".

Switzerland has set safety limits lower than the ICNIRP limits for certain "sensitive areas" (classrooms, for example).

In March 2020, for the first time since 1998, ICNIRP updated its guidelines for exposures to frequencies over 6 GHz, including the frequencies used for 5G that are over 6 GHz. The Commission added a restriction on acceptable levels of exposure to the whole body, added a restriction on acceptable levels for brief exposures to small regions of the body, and reduced the maximum amount of exposure permitted over a small region of the body.

Lawsuits

In the US, personal injury lawsuits have been filed by individuals against manufacturers (including Motorola,^[48] NEC, Siemens, and Nokia) on the basis of allegations of causation of brain cancer and death. In US federal courts, expert testimony relating to science must be first evaluated by a judge, in a Daubert hearing, to be relevant and valid before it is admissible as evidence. In a 2002 case against Motorola, the plaintiffs alleged that the use of wireless handheld telephones could cause brain cancer and that the use of Motorola phones caused one plaintiff's cancer. The judge ruled that no sufficiently reliable and relevant scientific evidence in support of either general or specific causation was proffered by the plaintiffs, accepted a motion to exclude the testimony of the plaintiffs' experts, and denied a motion to exclude the testimony of the defendants' experts.

Two separate cases in Italy, in 2009 and 2017, resulted in pensions being awarded to plaintiffs who had claimed their benign brain tumors were the result of prolonged mobile phone use in professional tasks, for 5–6 hours a day, which they ruled different from non-professional use.

In the UK Legal Action Against 5G sought a Judicial Review of the government's plan to deploy 5G. If successful, the group was to be represented by Michael Mansfield QC, a prominent British barrister. This application was denied on the basis that the government had demonstrated that 5G was as safe as 4G, and that the applicants had brought their action too late. 

Precautions

Precautionary principle

In 2000, the World Health Organization (WHO) recommended that the precautionary principle could be voluntarily adopted in this case. It follows the recommendations of the European Community for environmental risks.

According to the WHO, the "precautionary principle" is "a risk management policy applied in circumstances with a high degree of scientific uncertainty, reflecting the need to take action for a potentially serious risk without awaiting the results of scientific research." Other less stringent recommended approaches are prudent avoidance principle and as low as reasonably practicable. Although all of these are problematic in application, due to the widespread use and economic importance of wireless telecommunication systems in modern civilization, there is an increased popularity of such measures in the general public, though also evidence that such approaches may increase concern. They involve recommendations such as the minimization of usage, the limitation of use by at-risk population (e.g., children), the adoption of phones and microcells with as low as reasonably practicable levels of radiation, the wider use of hands-free and earphone technologies such as Bluetooth headsets, the adoption of maximal standards of exposure, RF field intensity and distance of base stations antennas from human habitations, and so forth. Overall, public information remains a challenge as various health consequences are evoked in the literature and by the media, putting populations under chronic exposure to potentially worrying information.

Precautionary measures and health advisories

In May 2011, the World Health Organization's International Agency for Research on Cancer announced it was classifying electromagnetic fields from mobile phones and other sources as "possibly carcinogenic to humans" and advised the public to adopt safety measures to reduce exposure, like use of hands-free devices or texting.

Some national radiation advisory authorities, including those of Austria, France, Germany, and Sweden, have recommended measures to minimize exposure to their citizens. Examples of the recommendations are:

• Use hands-free to decrease the radiation to the head.
• Keep the mobile phone away from the body.
• Do not use telephone in a car without an external antenna.

The use of "hands-free" was not recommended by the British Consumers' Association in a statement in November 2000, as they believed that exposure was increased. However, measurements for the (then) UK Department of Trade and Industry and others for the French Agence française de sécurité sanitaire environnementale [fr] showed substantial reductions. In 2005, Professor Lawrie Challis and others said clipping a ferrite bead onto hands-free kits stops the radio waves travelling up the wire and into the head.

Several nations have advised moderate use of mobile phones for children. A journal by Gandhi et al. in 2006 states that children receive higher levels of Specific Absorption Rate (SAR). When 5- and 10-year-olds are compared to adults, they receive about 153% higher SAR levels. Also, with the permittivity of the brain decreasing as one gets older and the higher relative volume of the exposed growing brain in children, radiation penetrates far beyond the mid-brain.

5G

Further information: 5G conspiracies

Further information: Misinformation related to 5G technology

See also: Misinformation related to the COVID-19 pandemic § 5G mobile phone networks

The FDA is quoted as saying that it "...continues to believe that the current safety limits for cellphone radiofrequency energy exposure remain acceptable for protecting the public health."

During the COVID-19 pandemic, misinformation circulated claiming that 5G networks contribute to the spread of COVID-19.

Bogus products

Products have been advertised that claim to shield people from EM radiation from mobile phones; in the US the Federal Trade Commission published a warning that "Scam artists follow the headlines to promote products that play off the news – and prey on concerned people."

According to the FTC, "there is no scientific proof that so-called shields significantly reduce exposure from electromagnetic emissions. Products that block only the earpiece – or another small portion of the phone – are totally ineffective because the entire phone emits electromagnetic waves." Such shields "may interfere with the phone's signal, cause it to draw even more power to communicate with the base station, and possibly emit more radiation." The FTC has enforced false advertising claims against companies that sell such products.

Cellular network

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Cellular_network 

 

Top of a cellular radio tower

 

Indoor cell site in Germany

 

Part of a series on
Antennas

A cellular network or mobile network is a communication network where the link to and from end nodes is wireless. The network is distributed over land areas called "cells", each served by at least one fixed-location transceiver (typically three cell sites or base transceiver stations). These base stations provide the cell with the network coverage which can be used for transmission of voice, data, and other types of content. A cell typically uses a different set of frequencies from neighboring cells, to avoid interference and provide guaranteed service quality within each cell.

When joined together, these cells provide radio coverage over a wide geographic area. This enables numerous portable transceivers (e.g., mobile phones, tablets and laptops equipped with mobile broadband modems, pagers, etc.) to communicate with each other and with fixed transceivers and telephones anywhere in the network, via base stations, even if some of the transceivers are moving through more than one cell during transmission.

Cellular networks offer a number of desirable features:

• More capacity than a single large transmitter, since the same frequency can be used for multiple links as long as they are in different cells
• Mobile devices use less power than with a single transmitter or satellite since the cell towers are closer
• Larger coverage area than a single terrestrial transmitter, since additional cell towers can be added indefinitely and are not limited by the horizon

Major telecommunications providers have deployed voice and data cellular networks over most of the inhabited land area of Earth. This allows mobile phones and mobile computing devices to be connected to the public switched telephone network and public Internet access. Private cellular networks can be used for research or for large organizations and fleets, such as dispatch for local public safety agencies or a taxicab company.

Concept

Example of frequency reuse factor or pattern 1/4

In a cellular radio system, a land area to be supplied with radio service is divided into cells in a pattern dependent on terrain and reception characteristics. These cell patterns roughly take the form of regular shapes, such as hexagons, squares, or circles although hexagonal cells are conventional. Each of these cells is assigned with multiple frequencies (f₁ – f₆) which have corresponding radio base stations. The group of frequencies can be reused in other cells, provided that the same frequencies are not reused in adjacent cells, which would cause co-channel interference.

The increased capacity in a cellular network, compared with a network with a single transmitter, comes from the mobile communication switching system developed by Amos Joel of Bell Labs that permitted multiple callers in a given area to use the same frequency by switching calls to the nearest available cellular tower having that frequency available. This strategy is viable because a given radio frequency can be reused in a different area for an unrelated transmission. In contrast, a single transmitter can only handle one transmission for a given frequency. Inevitably, there is some level of interference from the signal from the other cells which use the same frequency. Consequently, there must be at least one cell gap between cells which reuse the same frequency in a standard frequency-division multiple access (FDMA) system.

Consider the case of a taxi company, where each radio has a manually operated channel selector knob to tune to different frequencies. As drivers move around, they change from channel to channel. The drivers are aware of which frequency approximately covers some area. When they do not receive a signal from the transmitter, they try other channels until finding one that works. The taxi drivers only speak one at a time when invited by the base station operator. This is a form of time-division multiple access (TDMA).

History

See also: History of mobile phones

The first commercial cellular network, the 1G generation, was launched in Japan by Nippon Telegraph and Telephone (NTT) in 1979, initially in the metropolitan area of Tokyo. Within five years, the NTT network had been expanded to cover the whole population of Japan and became the first nationwide 1G network. It was an analog wireless network. The Bell System had developed cellular technology since 1947, and had cellular networks in operation in Chicago and Dallas prior to 1979, but commercial service was delayed by the breakup of the Bell System, with cellular assets transferred to the Regional Bell Operating Companies.

The wireless revolution began in the early 1990s, leading to the transition from analog to digital networks. This was enabled by advances in MOSFET technology. The MOSFET, originally invented by Mohamed M. Atalla and Dawon Kahng at Bell Labs in 1959, was adapted for cellular networks by the early 1990s, with the wide adoption of power MOSFET, LDMOS (RF amplifier), and RF CMOS (RF circuit) devices leading to the development and proliferation of digital wireless mobile networks.

The first commercial digital cellular network, the 2G generation, was launched in 1991. This sparked competition in the sector as the new operators challenged the incumbent 1G analog network operators.

Cell signal encoding

To distinguish signals from several different transmitters, frequency-division multiple access (FDMA, used by analog and D-AMPS systems), time-division multiple access (TDMA, used by GSM) and code-division multiple access (CDMA, first used for PCS, and the basis of 3G) were developed.

With FDMA, the transmitting and receiving frequencies used by different users in each cell are different from each other. Each cellular call was assigned a pair of frequencies (one for base to mobile, the other for mobile to base) to provide full-duplex operation. The original AMPS systems had 666 channel pairs, 333 each for the CLEC "A" system and ILEC "B" system. The number of channels was expanded to 416 pairs per carrier, but ultimately the number of RF channels limits the number of calls that a cell site could handle. Note that FDMA is a familiar technology to telephone companies, that used frequency-division multiplexing to add channels to their point-to-point wireline plants before time-division multiplexing rendered FDM obsolete.

With TDMA, the transmitting and receiving time slots used by different users in each cell are different from each other. TDMA typically uses digital signaling to store and forward bursts of voice data that are fit into time slices for transmission, and expanded at the receiving end to produce a somewhat normal-sounding voice at the receiver. TDMA must introduce latency (time delay) into the audio signal. As long as the latency time is short enough that the delayed audio is not heard as an echo, it is not problematic. Note that TDMA is a familiar technology for telephone companies, that used time-division multiplexing to add channels to their point-to-point wireline plants before packet switching rendered FDM obsolete.

The principle of CDMA is based on spread spectrum technology developed for military use during World War II and improved during the Cold War into direct-sequence spread spectrum that was used for early CDMA cellular systems and Wi-Fi. DSSS allows multiple simultaneous phone conversations to take place on a single wideband RF channel, without needing to channelize them in time or frequency. Although more sophisticated than older multiple access schemes (and unfamiliar to legacy telephone companies because it was not developed by Bell Labs), CDMA has scaled well to become the basis for 3G cellular radio systems.

Other available methods of multiplexing such as MIMO, a more sophisticated version of antenna diversity, combined with active beamforming provides much greater spatial multiplexing ability compared to original AMPS cells, that typically only addressed one to three unique spaces. Massive MIMO deployment allows much greater channel re-use, thus increasing the number of subscribers per cell site, greater data throughput per user, or some combination thereof. Quadrature Amplitude Modulation (QAM) modems offer an increasing number of bits per symbol, allowing more users per megahertz of bandwidth (and decibels of SNR), greater data throughput per user, or some combination thereof.

Frequency reuse

The key characteristic of a cellular network is the ability to re-use frequencies to increase both coverage and capacity. As described above, adjacent cells must use different frequencies, however, there is no problem with two cells sufficiently far apart operating on the same frequency, provided the masts and cellular network users' equipment do not transmit with too much power.

The elements that determine frequency reuse are the reuse distance and the reuse factor. The reuse distance, D is calculated as

${\displaystyle D=R{\sqrt {3N}}}$,

where R is the cell radius and N is the number of cells per cluster. Cells may vary in radius from 1 to 30 kilometres (0.62 to 18.64 mi). The boundaries of the cells can also overlap between adjacent cells and large cells can be divided into smaller cells.

The frequency reuse factor is the rate at which the same frequency can be used in the network. It is 1/K (or K according to some books) where K is the number of cells which cannot use the same frequencies for transmission. Common values for the frequency reuse factor are 1/3, 1/4, 1/7, 1/9 and 1/12 (or 3, 4, 7, 9 and 12 depending on notation).

In case of N sector antennas on the same base station site, each with different direction, the base station site can serve N different sectors. N is typically 3. A reuse pattern of N/K denotes a further division in frequency among N sector antennas per site. Some current and historical reuse patterns are 3/7 (North American AMPS), 6/4 (Motorola NAMPS), and 3/4 (GSM).

If the total available bandwidth is B, each cell can only use a number of frequency channels corresponding to a bandwidth of B/K, and each sector can use a bandwidth of B/NK.

Code-division multiple access-based systems use a wider frequency band to achieve the same rate of transmission as FDMA, but this is compensated for by the ability to use a frequency reuse factor of 1, for example using a reuse pattern of 1/1. In other words, adjacent base station sites use the same frequencies, and the different base stations and users are separated by codes rather than frequencies. While N is shown as 1 in this example, that does not mean the CDMA cell has only one sector, but rather that the entire cell bandwidth is also available to each sector individually.

Recently also orthogonal frequency-division multiple access based systems such as LTE are being deployed with a frequency reuse of 1. Since such systems do not spread the signal across the frequency band, inter-cell radio resource management is important to coordinate resource allocation between different cell sites and to limit the inter-cell interference. There are various means of inter-cell interference coordination (ICIC) already defined in the standard. Coordinated scheduling, multi-site MIMO or multi-site beamforming are other examples for inter-cell radio resource management that might be standardized in the future.

Directional antennas

Cellular telephone frequency reuse pattern. See U.S. Patent 4,144,411

Cell towers frequently use a directional signal to improve reception in higher-traffic areas. In the United States, the Federal Communications Commission (FCC) limits omnidirectional cell tower signals to 100 watts of power. If the tower has directional antennas, the FCC allows the cell operator to emit up to 500 watts of effective radiated power (ERP).

Although the original cell towers created an even, omnidirectional signal, were at the centers of the cells and were omnidirectional, a cellular map can be redrawn with the cellular telephone towers located at the corners of the hexagons where three cells converge. Each tower has three sets of directional antennas aimed in three different directions with 120 degrees for each cell (totaling 360 degrees) and receiving/transmitting into three different cells at different frequencies. This provides a minimum of three channels, and three towers for each cell and greatly increases the chances of receiving a usable signal from at least one direction.

The numbers in the illustration are channel numbers, which repeat every 3 cells. Large cells can be subdivided into smaller cells for high volume areas.

Cell phone companies also use this directional signal to improve reception along highways and inside buildings like stadiums and arenas.

Broadcast messages and paging

Practically every cellular system has some kind of broadcast mechanism. This can be used directly for distributing information to multiple mobiles. Commonly, for example in mobile telephony systems, the most important use of broadcast information is to set up channels for one-to-one communication between the mobile transceiver and the base station. This is called paging. The three different paging procedures generally adopted are sequential, parallel and selective paging.

The details of the process of paging vary somewhat from network to network, but normally we know a limited number of cells where the phone is located (this group of cells is called a Location Area in the GSM or UMTS system, or Routing Area if a data packet session is involved; in LTE, cells are grouped into Tracking Areas). Paging takes place by sending the broadcast message to all of those cells. Paging messages can be used for information transfer. This happens in pagers, in CDMA systems for sending SMS messages, and in the UMTS system where it allows for low downlink latency in packet-based connections.

Movement from cell to cell and handing over

In a primitive taxi system, when the taxi moved away from a first tower and closer to a second tower, the taxi driver manually switched from one frequency to another as needed. If communication was interrupted due to a loss of a signal, the taxi driver asked the base station operator to repeat the message on a different frequency.

In a cellular system, as the distributed mobile transceivers move from cell to cell during an ongoing continuous communication, switching from one cell frequency to a different cell frequency is done electronically without interruption and without a base station operator or manual switching. This is called the handover or handoff. Typically, a new channel is automatically selected for the mobile unit on the new base station which will serve it. The mobile unit then automatically switches from the current channel to the new channel and communication continues.

The exact details of the mobile system's move from one base station to the other vary considerably from system to system (see the example below for how a mobile phone network manages handover).

Mobile phone network

WCDMA network architecture

The most common example of a cellular network is a mobile phone (cell phone) network. A mobile phone is a portable telephone which receives or makes calls through a cell site (base station) or transmitting tower. Radio waves are used to transfer signals to and from the cell phone.

Modern mobile phone networks use cells because radio frequencies are a limited, shared resource. Cell-sites and handsets change frequency under computer control and use low power transmitters so that the usually limited number of radio frequencies can be simultaneously used by many callers with less interference.

A cellular network is used by the mobile phone operator to achieve both coverage and capacity for their subscribers. Large geographic areas are split into smaller cells to avoid line-of-sight signal loss and to support a large number of active phones in that area. All of the cell sites are connected to telephone exchanges (or switches), which in turn connect to the public telephone network.

In cities, each cell site may have a range of up to approximately 1⁄2 mile (0.80 km), while in rural areas, the range could be as much as 5 miles (8.0 km). It is possible that in clear open areas, a user may receive signals from a cell site 25 miles (40 km) away.

Since almost all mobile phones use cellular technology, including GSM, CDMA, and AMPS (analog), the term "cell phone" is in some regions, notably the US, used interchangeably with "mobile phone". However, satellite phones are mobile phones that do not communicate directly with a ground-based cellular tower but may do so indirectly by way of a satellite.

There are a number of different digital cellular technologies, including: Global System for Mobile Communications (GSM), General Packet Radio Service (GPRS), cdmaOne, CDMA2000, Evolution-Data Optimized (EV-DO), Enhanced Data Rates for GSM Evolution (EDGE), Universal Mobile Telecommunications System (UMTS), Digital Enhanced Cordless Telecommunications (DECT), Digital AMPS (IS-136/TDMA), and Integrated Digital Enhanced Network (iDEN). The transition from existing analog to the digital standard followed a very different path in Europe and the US. As a consequence, multiple digital standards surfaced in the US, while Europe and many countries converged towards the GSM standard.

Structure of the mobile phone cellular network

A simple view of the cellular mobile-radio network consists of the following:

• A network of radio base stations forming the base station subsystem.
• The core circuit switched network for handling voice calls and text
• A packet switched network for handling mobile data
• The public switched telephone network to connect subscribers to the wider telephony network

This network is the foundation of the GSM system network. There are many functions that are performed by this network in order to make sure customers get the desired service including mobility management, registration, call set-up, and handover.

Any phone connects to the network via an RBS (Radio Base Station) at a corner of the corresponding cell which in turn connects to the Mobile switching center (MSC). The MSC provides a connection to the public switched telephone network (PSTN). The link from a phone to the RBS is called an uplink while the other way is termed downlink.

Radio channels effectively use the transmission medium through the use of the following multiplexing and access schemes: frequency-division multiple access (FDMA), time-division multiple access (TDMA), code-division multiple access (CDMA), and space-division multiple access (SDMA).

Small cells

Main article: Small cell

Small cells, which have a smaller coverage area than base stations, are categorised as follows:

• Microcell -> less than 2 kilometres,
• Picocell -> less than 200 metres,
• Femtocell -> around 10 metres,
• Attocell -> 1–4 metres

Cellular handover in mobile phone networks

Main article: Handover

As the phone user moves from one cell area to another cell while a call is in progress, the mobile station will search for a new channel to attach to in order not to drop the call. Once a new channel is found, the network will command the mobile unit to switch to the new channel and at the same time switch the call onto the new channel.

With CDMA, multiple CDMA handsets share a specific radio channel. The signals are separated by using a pseudonoise code (PN code) that is specific to each phone. As the user moves from one cell to another, the handset sets up radio links with multiple cell sites (or sectors of the same site) simultaneously. This is known as "soft handoff" because, unlike with traditional cellular technology, there is no one defined point where the phone switches to the new cell.

In IS-95 inter-frequency handovers and older analog systems such as NMT it will typically be impossible to test the target channel directly while communicating. In this case, other techniques have to be used such as pilot beacons in IS-95. This means that there is almost always a brief break in the communication while searching for the new channel followed by the risk of an unexpected return to the old channel.

If there is no ongoing communication or the communication can be interrupted, it is possible for the mobile unit to spontaneously move from one cell to another and then notify the base station with the strongest signal.

Cellular frequency choice in mobile phone networks

Main article: Cellular frequencies

The effect of frequency on cell coverage means that different frequencies serve better for different uses. Low frequencies, such as 450  MHz NMT, serve very well for countryside coverage. GSM 900 (900 MHz) is suitable for light urban coverage. GSM 1800 (1.8  GHz) starts to be limited by structural walls. UMTS, at 2.1 GHz is quite similar in coverage to GSM 1800.

Higher frequencies are a disadvantage when it comes to coverage, but it is a decided advantage when it comes to capacity. Picocells, covering e.g. one floor of a building, become possible, and the same frequency can be used for cells which are practically neighbors.

Cell service area may also vary due to interference from transmitting systems, both within and around that cell. This is true especially in CDMA based systems. The receiver requires a certain signal-to-noise ratio, and the transmitter should not send with too high transmission power in view to not cause interference with other transmitters. As the receiver moves away from the transmitter, the power received decreases, so the power control algorithm of the transmitter increases the power it transmits to restore the level of received power. As the interference (noise) rises above the received power from the transmitter, and the power of the transmitter cannot be increased anymore, the signal becomes corrupted and eventually unusable. In CDMA-based systems, the effect of interference from other mobile transmitters in the same cell on coverage area is very marked and has a special name, cell breathing.

One can see examples of cell coverage by studying some of the coverage maps provided by real operators on their web sites or by looking at independently crowdsourced maps such as Opensignal or CellMapper. In certain cases they may mark the site of the transmitter; in others, it can be calculated by working out the point of strongest coverage.

A cellular repeater is used to extend cell coverage into larger areas. They range from wideband repeaters for consumer use in homes and offices to smart or digital repeaters for industrial needs.

Cell size

The following table shows the dependency of the coverage area of one cell on the frequency of a CDMA2000 network:

Frequency (MHz)	Cell radius (km)	Cell area (km2)	Relative cell count
450	48.9	7521	1
950	26.9	2269	3.3
1800	14.0	618	12.2
2100	12.0	449	16.2

Delayed sleep phase disorder

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Delayed_sleep_phase_disorder 

Delayed sleep phase disorder
Other names	Delayed sleep–wake phase disorder, delayed sleep phase syndrome, delayed sleep phase type
Comparison of standard (green) and DSPD (blue) circadian rhythms
Specialty	Psychiatry, sleep medicine

Delayed sleep phase disorder (DSPD), more often known as delayed sleep phase syndrome and also as delayed sleep–wake phase disorder, is a chronic dysregulation of a person's circadian rhythm (biological clock), compared to those of the general population and societal norms. The disorder affects the timing of sleep, peak period of alertness, the core body temperature, rhythm, hormonal as well as other daily cycles. People with DSPD generally fall asleep some hours after midnight and have difficulty waking up in the morning. People with DSPD probably have a circadian period significantly longer than 24 hours. Depending on the severity, the symptoms can be managed to a greater or lesser degree, but no cure is known, and research suggests a genetic origin for the disorder.

Affected people often report that while they do not get to sleep until the early morning, they do fall asleep around the same time every day. Unless they have another sleep disorder such as sleep apnea in addition to DSPD, patients can sleep well and have a normal need for sleep. However, they find it very difficult to wake up in time for a typical school or work day. If they are allowed to follow their own schedules, e.g. sleeping from 4:00 am to 1:00 pm, their sleep is improved and they may not experience excessive daytime sleepiness. Attempting to force oneself onto daytime society's schedule with DSPD has been compared to constantly living with jet lag; DSPD has been called "social jet lag".

Researchers in 2017 linked DSPD to at least one genetic mutation. The syndrome usually develops in early childhood or adolescence. An adolescent version may disappear in late adolescence or early adulthood; otherwise, DSPD is a lifelong condition. The best estimate of prevalence among adults is 0.13–0.17% (1 in 600). Prevalence among adolescents is as much as 7–16%.

DSPD was first formally described in 1981 by Elliot D. Weitzman and others at Montefiore Medical Center.^[9] It is responsible for 7–13% of patient complaints of chronic insomnia. However, since many doctors are unfamiliar with the condition, it often goes untreated or is treated inappropriately; DSPD is often misdiagnosed as primary insomnia or as a psychiatric condition. DSPD can be treated or helped in some cases by careful daily sleep practices, morning light therapy, evening dark therapy, earlier exercise and meal times, and medications such as aripiprazole, melatonin, and modafinil; melatonin is a natural neurohormone partly responsible for the human body clock. At its most severe and inflexible, DSPD is a disability. A chief difficulty of treating DSPD is in maintaining an earlier schedule after it has been established, as the patient's body has a strong tendency to reset the sleeping schedule to its intrinsic late times. People with DSPD may improve their quality of life by choosing careers that allow late sleeping times, rather than forcing themselves to follow a conventional 9-to-5 work schedule.

Presentation

Comorbidity

Depression

In the DSPD cases reported in the literature, about half of the patients have suffered from clinical depression or other psychological problems, about the same proportion as among patients with chronic insomnia. According to the ICSD:

Although some degree of psychopathology is present in about half of adult patients with DSPD, there appears to be no particular psychiatric diagnostic category into which these patients fall. Psychopathology is not particularly more common in DSPD patients compared to patients with other forms of "insomnia." ... Whether DSPD results directly in clinical depression, or vice versa, is unknown, but many patients express considerable despair and hopelessness over sleeping normally again.

A direct neurochemical relationship between sleep mechanisms and depression is another possibility.

It is conceivable that DSPD has a role in causing depression because it can be such a stressful and misunderstood disorder. A 2008 study from the University of California, San Diego found no association of bipolar disorder (history of mania) with DSPD, and it states that

there may be behaviorally-mediated mechanisms for comorbidity between DSPD and depression. For example, the lateness of DSPD cases and their unusual hours may lead to social opprobrium and rejection, which might be depressing.

The fact that half of DSPD patients are not depressed indicates that DSPD is not merely a symptom of depression. Sleep researcher Michael Terman has suggested that those who follow their internal circadian clocks may be less likely to suffer from depression than those trying to live on a different schedule.

DSPD patients who also suffer from depression may be best served by seeking treatment for both problems. There is some evidence that effectively treating DSPD can improve the patient's mood and make antidepressants more effective.

Vitamin D deficiency has been linked to depression. As it is a condition which comes from lack of exposure to sunlight, anyone who does not get enough sunlight exposure during daylight hours (about 20 to 30 minutes three times a week, depending on skin tone, latitude, and the time of year) could be at risk, without adequate dietary sources or supplements.

Attention deficit hyperactivity disorder

DSPD is genetically linked to attention deficit hyperactivity disorder by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm and a high proportion of DSPD among those with ADHD.

Overweight

A 2019 study from Boston showed a relationship of evening chronotypes and greater social jet lag with greater body weight / adiposity in adolescent girls, but not boys, independent of sleep duration.

Obsessive–compulsive disorder

Persons with obsessive–compulsive disorder are also diagnosed with DSPD at a much higher rate than the general public.

Mechanism

Main article: Circadian rhythm sleep disorder

DSPD is a disorder of the body's timing system—the biological clock. Individuals with DSPD might have an unusually long circadian cycle, might have a reduced response to the resetting effect of daylight on the body clock, and/or may respond overly to the delaying effects of evening light and too little to the advancing effect of light earlier in the day. In support of the increased sensitivity to evening light hypothesis, "the percentage of melatonin suppression by a bright light stimulus of 1,000 lux administered 2 hours prior to the melatonin peak has been reported to be greater in 15 DSPD patients than in 15 controls."

The altered phase relationship between the timing of sleep and the circadian rhythm of body core temperature has been reported previously in DSPD patients studied in entrained conditions. That such an alteration has also been observed in temporal isolation (free-running clock) supports the notion that the etiology of DSPD goes beyond simply a reduced capacity to achieve and maintain the appropriate phase relationship between sleep timing and the 24-hour day. Rather, the disorder may also reflect a fundamental inability of the endogenous circadian timing system to maintain normal internal phase relationships among physiological systems, and to properly adjust those internal relationships within the confines of the 24-hour day. In normal subjects, the phase relationship between sleep and temperature changes in temporal isolation relative to that observed under entrained conditions: in isolation, tmin tends to occur toward the beginning of sleep, whereas under entrained conditions, tmin occurs toward the end of the sleep period—a change in phase angle of several hours; DSPD patients may have a reduced capacity to achieve such a change in phase angle in response to entrainment.

Possibly as a consequence of these altered internal phase relationships, that the quality of sleep in DSPD may be substantially poorer than that of normal subjects, even when bedtimes and wake times are self-selected. A DSPD subject exhibited an average sleep onset latency twice that of the 3 control subjects and almost twice the amount of wakefulness after sleep onset (WASO) as control subjects, resulting in significantly poorer sleep efficiency. Also, the temporal distribution of slow wave sleep was significantly altered in the DSPD subject. This finding may suggest that, in addition to abnormal circadian clock function, DSPD may be characterized by alteration(s) in the homeostatic regulation of sleep, as well. Specifically, the rate with which Process S is depleted during sleep may be slowed. This could, conceivably, contribute to the excessive sleep inertia upon awakening that is often reported by DSPD sufferers. It has also been hypothesized that, due to the altered phase angle between sleep and temperature observed in DSPD, and the tendency for longer sleep periods, these individuals may simply sleep through the phase-advance portion of the light PRC. Though quite limited in terms of the total number of DSPD patients studied, such data seem to contradict the notion that DSPD is merely a disorder of sleep timing, rather than a disorder of the sleep system itself.

People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically help to advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPD have difficulty falling asleep before their usual sleep time, even if they are sleep-deprived. Sleep deprivation does not reset the circadian clock of DSPD patients, as it does with normal people.

People with the disorder who try to live on a normal schedule cannot fall asleep at a "reasonable" hour and have extreme difficulty waking because their biological clocks are not in phase with that schedule. Non-DSPD people who do not adjust well to working a night shift have similar symptoms (diagnosed as shift-work sleep disorder).

In most cases, it is not known what causes the abnormality in the biological clocks of DSPD patients. DSPD tends to run in families, and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene and CRY1 gene. There have been several documented cases of DSPD and non-24-hour sleep–wake disorder developing after traumatic head injury. There have been cases of DSPD developing into non-24-hour sleep–wake disorder, a severe and debilitating disorder in which the individual sleeps later each day.

Diagnosis

A sleep diary with nighttime at the top and the weekend in the middle, to better notice trends

DSPD is diagnosed by a clinical interview, actigraphic monitoring, and/or a sleep diary kept by the patient for at least two weeks. When polysomnography is also used, it is primarily for the purpose of ruling out other disorders such as narcolepsy or sleep apnea.

DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder. DSPD is often confused with: psychophysiological insomnia; depression; psychiatric disorders such as schizophrenia, ADHD or ADD; other sleep disorders; or school refusal. Practitioners of sleep medicine point out the dismally low rate of accurate diagnosis of the disorder, and have often asked for better physician education on sleep disorders.

Definition

According to the International Classification of Sleep Disorders, Revised (ICSD-R, 2001), the circadian rhythm sleep disorders share a common underlying chronophysiologic basis:

The major feature of these disorders is a misalignment between the patient's sleep-wake pattern and the pattern that is desired or regarded as the societal norm... In most circadian rhythm sleep disorders, the underlying problem is that the patient cannot sleep when sleep is desired, needed or expected.

Incorporating minor updates (ICSD-3, 2014), the diagnostic criteria for delayed sleep phase disorder are:

1. An intractable delay in the phase of the major sleep period occurs in relation to the desired clock time, as evidenced by a chronic or recurrent (for at least three months) complaint of inability to fall asleep at a desired conventional clock time together with the inability to awaken at a desired and socially acceptable time.
2. When not required to maintain a strict schedule, patients exhibit improved sleep quality and duration for their age and maintain a delayed phase of entrainment to local time.
3. Patients have little or no reported difficulty in maintaining sleep once sleep has begun.
4. Patients have a relatively severe to absolute inability to advance the sleep phase to earlier hours by enforcing conventional sleep and wake times.
5. Sleep–wake logs and/or actigraphy monitoring for at least two weeks document a consistent habitual pattern of sleep onsets, usually later than 2 am, and lengthy sleeps.
6. Occasional noncircadian days may occur (i.e., sleep is "skipped" for an entire day and night plus some portion of the following day), followed by a sleep period lasting 12 to 18 hours.
7. The symptoms do not meet the criteria for any other sleep disorder causing inability to initiate sleep or excessive sleepiness.
8. If one of the following laboratory methods is used, it must demonstrate a significant delay in the timing of the habitual sleep period: 1) 24-hour polysomnographic monitoring (or two consecutive nights of polysomnography and an intervening multiple sleep latency test), 2) Continuous temperature monitoring showing that the time of the absolute temperature nadir is delayed into the second half of the habitual (delayed) sleep episode.

Some people with the condition adapt their lives to the delayed sleep phase, avoiding morning business hours as much as possible. The ICSD's severity criteria are:

• Mild: Two-hour delay (relative to the desired sleep time) associated with little or mild impairment of social or occupational functioning.
• Moderate: Three-hour delay associated with moderate impairment.
• Severe: Four-hour delay associated with severe impairment.

Some features of DSPD which distinguish it from other sleep disorders are:

• People with DSPD have at least a normal—and often much greater than normal—ability to sleep during the morning, and sometimes in the afternoon as well. In contrast, those with chronic insomnia do not find it much easier to sleep during the morning than at night.
• People with DSPD fall asleep at more or less the same time every night, and sleep comes quite rapidly if the person goes to bed near the time they usually fall asleep. Young children with DSPD resist going to bed before they are sleepy, but the bedtime struggles disappear if they are allowed to stay up until the time they usually fall asleep.
• DSPD patients usually sleep well and regularly when they can follow their own sleep schedule, e.g., on weekends and during vacations.
• DSPD is a chronic condition. Symptoms must have been present for at least three months before a diagnosis of DSPD can be made.

Often people with DSPD manage only a few hours sleep per night during the working week, then compensate by sleeping until the afternoon on weekends. Sleeping late on weekends, and/or taking long naps during the day, may give people with DSPD relief from daytime sleepiness but may also perpetuate the late sleep phase.

People with DSPD can be called "night owls". They feel most alert and say they function best and are most creative in the evening and at night. People with DSPD cannot simply force themselves to sleep early. They may toss and turn for hours in bed, and sometimes not sleep at all, before reporting to work or school. Less-extreme and more-flexible night owls are within the normal chronotype spectrum.

By the time those who have DSPD seek medical help, they usually have tried many times to change their sleeping schedule. Failed tactics to sleep at earlier times may include maintaining proper sleep hygiene, relaxation techniques, early bedtimes, hypnosis, alcohol, sleeping pills, dull reading, and home remedies. DSPD patients who have tried using sedatives at night often report that the medication makes them feel tired or relaxed, but that it fails to induce sleep. They often have asked family members to help wake them in the morning, or they have used multiple alarm clocks. As the disorder occurs in childhood and is most common in adolescence, it is often the patient's parents who initiate seeking help, after great difficulty waking their child in time for school.

The current formal name established in the third edition of the International Classification of Sleep Disorders (ICSD-3) is delayed sleep-wake phase disorder. Earlier, and still common, names include delayed sleep phase disorder (DSPD), delayed sleep phase syndrome (DSPS), and circadian rhythm sleep disorder, delayed sleep phase type (DSPT).

Management

Treatment, a set of management techniques, is specific to DSPD. It is different from treatment of insomnia, and recognizes the patients' ability to sleep well on their own schedules, while addressing the timing problem. Success, if any, may be partial; for example, a patient who normally awakens at noon may only attain a wake time of 10 or 10:30 with treatment and follow-up. Being consistent with the treatment is paramount.

Before starting DSPD treatment, patients are often asked to spend at least a week sleeping regularly, without napping, at the times when the patient is most comfortable. It is important for patients to start treatment well-rested.

Non-pharmacological

One treatment strategy is light therapy (phototherapy), with either a bright white lamp providing 10,000 lux at a specified distance from the eyes or a wearable LED device providing 350–550 lux at a shorter distance. Sunlight can also be used. The light is typically timed for 30–90 minutes at the patient's usual time of spontaneous awakening, or shortly before (but not long before), which is in accordance with the phase response curve (PRC) for light. Only experimentation, preferably with specialist help, will show how great an advance is possible and comfortable. For maintenance, some patients must continue the treatment indefinitely; some may reduce the daily treatment to 15 minutes; others may use the lamp, for example, just a few days a week or just every third week. Whether the treatment is successful is highly individual. Light therapy generally requires adding some extra time to the patient's morning routine. Patients with a family history of macular degeneration are advised to consult with an eye doctor. The use of exogenous melatonin administration (see below) in conjunction with light therapy is common.

Light restriction in the evening, sometimes called darkness therapy or scototherapy, is another treatment strategy. Just as bright light upon awakening should advance one's sleep phase, bright light in the evening and night delays it (see the PRC). It is suspected that DSPD patients may be overly sensitive to evening light. The photopigment of the retinal photosensitive ganglion cells, melanopsin, is excited by light mainly in the blue portion of the visible spectrum (absorption peaks at ~480 nanometers).

A formerly popular treatment, phase delay chronotherapy, is intended to reset the circadian clock by manipulating bedtimes. It consists of going to bed two or more hours later each day for several days until the desired bedtime is reached, and it often must be repeated every few weeks or months to maintain results. Its safety is uncertain, notably because it has led to the development of non-24-hour sleep-wake rhythm disorder, a much more severe disorder.

A modified chronotherapy is called controlled sleep deprivation with phase advance, SDPA. One stays awake one whole night and day, then goes to bed 90 minutes earlier than usual and maintains the new bedtime for a week. This process is repeated weekly until the desired bedtime is reached.

Earlier exercise and meal times can also help promote earlier sleep times.

Pharmacological

Aripiprazole (brand name Abilify) is an atypical antipsychotic that has been shown to be effective in treating DSPD by advancing sleep onset, sleep midpoint, and sleep offset at relatively low doses.

Phase response curves for light and for melatonin administration

Melatonin taken an hour or so before the usual bedtime may induce sleepiness. Taken this late, it does not, of itself, affect circadian rhythms, but a decrease in exposure to light in the evening is helpful in establishing an earlier pattern. In accordance with its phase response curve (PRC), a very small dose of melatonin can also, or instead, be taken some hours earlier as an aid to resetting the body clock; it must then be small enough not to induce excessive sleepiness.

Side effects of melatonin may include sleep disturbance, nightmares, daytime sleepiness, and depression, though the current tendency to use lower doses has decreased such complaints. Large doses of melatonin can even be counterproductive: Lewy et al. provide support to "the idea that too much melatonin may spill over onto the wrong zone of the melatonin phase-response curve." The long-term effects of melatonin administration have not been examined. In some countries, the hormone is available only by prescription or not at all. In the United States and Canada, melatonin is on the shelf of most pharmacies and herbal stores. The prescription drug Rozerem (ramelteon) is a melatonin analogue that selectively binds to the melatonin MT₁ and MT₂ receptors and, hence, has the possibility of being effective in the treatment of DSPD.

A review by the US Department of Health and Human Services found little difference between melatonin and placebo for most primary and secondary sleep disorders. The one exception, where melatonin is effective, is the "circadian abnormality" DSPD. Another systematic review found inconsistent evidence for the efficacy of melatonin in treating DSPD in adults, and noted that it was difficult to draw conclusions about its efficacy because many recent studies on the subject were uncontrolled.

Modafinil (brand name Provigil) is a stimulant approved in the US for treatment of shift-work sleep disorder, which shares some characteristics with DSPD. A number of clinicians prescribe it for DSPD patients, as it may improve a sleep-deprived patient's ability to function adequately during socially desirable hours. It is generally not recommended to take modafinil after noon; modafinil is a relatively long-acting drug with a half-life of 15 hours, and taking it during the later part of the day can make it harder to fall asleep at bedtime.

Vitamin B₁₂ was, in the 1990s, suggested as a remedy for DSPD, and is still recommended by some sources. Several case reports were published. However, a review for the American Academy of Sleep Medicine in 2007 concluded that no benefit was seen from this treatment.

Prognosis

Risk of relapse

A strict schedule and good sleep hygiene are essential in maintaining any good effects of treatment. With treatment, some people with mild DSPD may sleep and function well with an earlier sleep schedule. Caffeine and other stimulant drugs to keep a person awake during the day may not be necessary and should be avoided in the afternoon and evening, in accordance with good sleep hygiene. A chief difficulty of treating DSPD is in maintaining an earlier schedule after it has been established. Inevitable events of normal life, such as staying up late for a celebration or deadline, or having to stay in bed with an illness, tend to reset the sleeping schedule to its intrinsic late times.

Long-term success rates of treatment have seldom been evaluated. However, experienced clinicians acknowledge that DSPD is extremely difficult to treat. One study of 61 DSPD patients, with average sleep onset at about 3:00 am and average waking time of about 11:30 am, was followed with questionnaires to the subjects after a year. Good effect was seen during the six-week treatment with a large daily dose of melatonin. After ceasing melatonin use over 90% had relapsed to pre-treatment sleeping patterns within the year, 29% reporting that the relapse occurred within one week. The mild cases retained changes significantly longer than the severe cases.

Adaptation to late sleeping times

Working the evening or night shift, or working at home, makes DSPD less of an obstacle for some. Many of these people do not describe their pattern as a "disorder". Some DSPD individuals nap, even taking 4–5 hours of sleep in the morning and 4–5 in the evening. DSPD-friendly careers can include security work, the entertainment industry, hospitality work in restaurants, theaters, hotels or bars, call center work, manufacturing, healthcare or emergency medicine, commercial cleaning, taxi or truck driving, the media, and freelance writing, translation, IT work, or medical transcription. Some other careers that have an emphasis on early morning work hours, such as bakers, coffee baristas, pilots and flight crews, teachers, mail carriers, waste collection, and farming, can be particularly difficult for people who naturally sleep later than is typical. Some careers, such as over-the-road truck drivers, firefighters, law enforcement, nursing, can be suitable for both people with delayed sleep phase syndrome and people with the opposite condition, advanced sleep phase disorder, as these workers are needed both very early in the morning and also late at night.

Some people with the disorder are unable to adapt to earlier sleeping times, even after many years of treatment. Sleep researchers Dagan and Abadi have proposed that the existence of untreatable cases of DSPD be formally recognized as a "sleep-wake schedule disorder (SWSD) disability", an invisible disability.

Rehabilitation for DSPD patients includes acceptance of the condition and choosing a career that allows late sleeping times or running a home business with flexible hours. In a few schools and universities, students with DSPD have been able to arrange to take exams at times of day when their concentration levels may be good.

Patients suffering from SWSD disability should be encouraged to accept the fact that they suffer from a permanent disability, and that their quality of life can only be improved if they are willing to undergo rehabilitation. It is imperative that physicians recognize the medical condition of SWSD disability in their patients and bring it to the notice of the public institutions responsible for vocational and social rehabilitation.

In the United States, the Americans with Disabilities Act requires that employers make reasonable accommodations for employees with sleeping disorders. In the case of DSPD, this may require that the employer accommodate later working hours for jobs normally performed on a "9 to 5" work schedule. The statute defines "disability" as a "physical or mental impairment that substantially limits one or more major life activities", and Section 12102(2)(a) itemizes sleeping as a "major life activity".

Impact on patients

Lack of public awareness of the disorder contributes to the difficulties experienced by people with DSPD, who are commonly stereotyped as undisciplined or lazy. Parents may be chastised for not giving their children acceptable sleep patterns, and schools and workplaces rarely tolerate chronically late, absent, or sleepy students and workers, failing to see them as having a chronic illness.

By the time DSPD sufferers receive an accurate diagnosis, they often have been misdiagnosed or labelled as lazy and incompetent workers or students for years. Misdiagnosis of circadian rhythm sleep disorders as psychiatric conditions causes considerable distress to patients and their families, and leads to some patients being inappropriately prescribed psychoactive drugs. For many patients, diagnosis of DSPD is itself a life-changing breakthrough.

As DSPD is so little-known and so misunderstood, peer support may be important for information, self-acceptance, and future research studies.

People with DSPD who force themselves to follow a normal 9–5 workday "are not often successful and may develop physical and psychological complaints during waking hours, e.g., sleepiness, fatigue, headache, decreased appetite, or depressed mood. Patients with circadian rhythm sleep disorders often have difficulty maintaining ordinary social lives, and some of them lose their jobs or fail to attend school."

Epidemiology

There have been several studies that have attempted to estimate the prevalence of DSPD. Results vary due to differences in methods of data collection and diagnostic criteria. A particular issue is where to draw the line between extreme evening chronotypes and clinical DSPD. Using the ICSD-1 diagnostic criteria (current edition ICSD-3) a study by telephone questionnaire in 1993 of 7,700 randomly selected adults (aged 18–67) in Norway estimated the prevalence of DSPD at 0.17%. A similar study in 1999 of 1,525 adults (aged 15–59) in Japan estimated its prevalence at 0.13%. A somewhat higher prevalence of 0.7% was found in a 1995 San Diego study. A 2014 study of 9100 New Zealand adults (age 20–59) using a modified version of the Munich Chronotype Questionnaire found a DSPD prevalence of 1.5% to 8.9% depending on the strictness of the definition used. A 2002 study of older adults (age 40–65) in San Diego found 3.1% had complaints of difficulty falling asleep at night and waking in the morning, but did not apply formal diagnostic criteria. Actimetry readings showed only a small proportion of this sample had delays of sleep timing.

A marked delay of sleep patterns is a normal feature of the development of adolescent humans. According to Mary Carskadon, both circadian phase and homeostasis (the accumulation of sleep pressure during the wake period) contribute to a DSPD-like condition in post-pubertal as compared to pre-pubertal youngsters. Adolescent sleep phase delay "is present both across cultures and across mammalian species" and "it seems to be related to pubertal stage rather than age." As a result, diagnosable DSPD is much more prevalent among adolescents. with estimates ranging from 3.4% to 8.4% among high school students.